How T-Cell recognizes a cell infected by a virus?

How T-Cell recognizes a cell infected by a virus?

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According to few articles I read (like BBC about The people with hidden immunity against Covid-19 ):

starting out about four or five days after infection, you begin to see T cells getting activated, and indications they are specifically recognising cells infected with the virus,” says Hayday. These unlucky cells are then dispatched quickly and brutally - either directly by the T cells themselves, or by other parts of the immune system they recruit to do the unpleasant task for them - before the virus has a chance to turn them into factories that churn out more copies of itself.

When virus just entered a cell, but had no chance to churn more copies: Is surface of the cell any different? How T-cell can distinguish infected cell from non-infected?

I am no biologist, but I am fascinated about biology now, and curious to learn more. Sorry if I am not using proper terminology.

I found How do T-cells determine which cells they've already inspected? , but T-cell activation is mentioned only in the context of dendritic cells and lymph nodes. IIUC, T-cells should attack lungs cells to eliminate cells infected by covid-19 there.

All cells chew up internal proteins all the time - it's part of the normal activity of cells to recycle those proteins into amino acids to be rebuilt into other proteins. The first step is chopping up the protein into peptides by the proteasome.

When a virus infects a cell, one key thing it needs to do to replicate is to have the cell start making viral proteins. However, some of these get chewed up, too.

Some of the peptide fragments get bound to major histocompatibility complex class 1 (MHC-1) molecules. These are then transported to the cell surface. This is the cell advertising "hey, this is what I've found in the trash lately."

Sort of like antibodies, T-cells only bind certain antigens, and during development the immune system learns which antigens are self versus foreign by process of elimination: if you detect it during development, it must be yours. Everything else is fair game to attack. When a killer T-cell binds strongly to the MHC-1:peptide complex, it recognizes that this is a foreign peptide and the cell presenting it must be infected or damaged in some way, and this starts a cascade that leads to apoptosis of the infected cell.

The Role of T Cells in the Body

T cells are a type of white blood cell known as a lymphocyte. Lymphocytes protect the body against cancerous cells and cells that have become infected by pathogens, such as bacteria and viruses. T cell lymphocytes develop from stem cells in bone marrow. These immature T cells migrate to the thymus via the blood. The thymus is a lymphatic system gland that functions mainly to promote the development of mature T cells. In fact, the "T " in T cell lymphocyte stands for thymus derived.

T cell lymphocytes are necessary for cell mediated immunity, which is an immune response that involves the activation of immune cells to fight infection. T cells function to actively destroy infected cells, as well as to signal other immune cells to participate in the immune response.

Key Takeaways: T Cells

  • T cells are lymphocyte immune cells that protect the body from pathogens and cancer cells.
  • T cells originate from bone marrow and mature in the thymus. They are important for cell mediated immunity and the activation of immune cells to fight infection.
  • Cytotoxic T cells actively destroy infected cells through the use of granule sacs that contain digestive enzymes.
  • Helper T cells activate cytotoxic T cells, macrophages, and stimulate antibody production by B cell lymphocytes.
  • Regulatory T cells suppress the actions of B and T cells to decrease the immune response when a highly active response is no longer warranted.
  • Natural Killer T cells distinguish infected or cancerous cells from normal body cells and attack cells that do not contain molecular markers that identify them as body cells.
  • Memory T cells protect against previously encountered antigens and may provide lifetime protection against some pathogens.

What are T cells and how do they help immunity?

T cells might play a crucial role in COVID-19 vaccines efficacy against variants.

COVID-19 vaccines currently rolled out worldwide induce a potent antibody response, protecting vaccinated people against severe disease and death.

The antibodies that vaccines generate act against the spike protein SARS-CoV2 uses to invade our cells. But as variants emerge, there are concerns that antibodies’ reduced ability to stop the infection will make vaccines less effective.

The immune response is a team effort

Vaccine-induced antibodies are our first line of defence against the virus as it enters our body. They sit in our airways and float in our blood. As they encounter the virus, they immediately recognise and neutralise its spike protein blocking it from invading our cells.

To effectively prevent infection, antibodies need to match the spike protein. If this varies even slightly, antibodies might not recognise it, and the virus is free to make its way to cells and replicate.

Current COVID-19 vaccines are based on the original strain first identified in Wuhan, so they elicit antibodies that perfectly fit the spike protein of that strain. However, variants of concern have slightly changed the spike protein, so scientists worry that vaccine-induced antibodies might not stick perfectly to the mutant spikes and lose efficacy.

Fortunately, antibodies are not the only immune response vaccines can elicit. There are T cells, too.

When antibodies wane over time or are not effective against a specific variant, some cells are infected. That is when T cells come to the rescue.

These cells sit in our lymph nodes – the glands under the arms, and at the base of the neck, that are part of our immune system. During a viral infection, T cells can identify cells that have been infected and kill them. This mechanism prevents severe disease and ends the infection. But, unlike antibodies, it takes a few days before T cells kick in.

While antibodies limit infection, T cells clear the virus-infected cells. “It’s a team effort,” says Professor Stephanie Gras, a molecular biologist at La Trobe University.

The result is a mild or asymptomatic infection, unlikely to be transmitted to others. “T cell responses can be really important because they can ameliorate the symptoms of infection,” says Professor Nicole La Gruta, a T cell expert at Monash University.

How T cells work

In a natural infection, a virus enters a cell, seizes its machinery and starts replicating itself. However, the invaded cells can sneakily flag the invader’s presence by sticking many random fragments of the virus on its membrane. T cells recognise these flags and kill the cell to stop virus replication.

COVID-19 vaccines that contain inactivated virus or spike protein cannot produce a T cells response, explains La Gruta. But other vaccines, such as AstraZeneca and Pfizer, require cells to produce the spike protein. The exact flagging mechanism occurs – cells stick fragments of the spike on their membrane to alert the immune system. T cells activate, but the low dose of the vaccine is just enough to teach them what to look out for without triggering an infection.

“Vaccines educate your T cells to recognise these small part of the protein,” says Gras. “So if you do get an infection, the T cells keep the memory of having seen those type of protein once before and can be activated much faster.”

Will T cells save us from variants?

Unlike antibodies, T cells are good at recognising variations of the virus fragments, says Gras. That might explain why T cells generated in vaccinated people can recognise and are effective against variants of concern.

It might also explain why some COVID-19 vaccines can effectively prevent severe symptoms and death even in regions where variants circulate widely. In some cases, vaccine-induced antibodies have reduced ability to prevent infection with some variants. Nonetheless, the vaccines prevent severe disease and death because T cells can still recognise variant virus-infected cells and clear them.

T cell response is difficult to gauge, but current evidence is encouraging

T cell response is hard to measure, says La Gruta.

Antibodies generated in different people who have received the same vaccine are the same because they target the same antigen – the spike protein.

T cells target a whole range of antigens – the virus fragments that invaded cells flag on their membrane. The selection of these fragments is dictated by our genetics. That means that people who have received the same vaccine might flag different fragments, so their T cell response is different.

Assays to measure T cell response require large blood samples from patients and can be complex and costly to perform.

But recent studies showing a strong T cell response in patients who have recovered from COVID-19 nine months after infection are encouraging.

Another study showed that patients who recovered from SARS – the disease associated with SARS-CoV infection – had T cells able to recognise SARS-CoV 17 years after the SARS outbreak in 2003.

“There is good hope that we will be protected for a long time,” says Gras.

The T cell response some vaccines elicit might not stop us from getting infected with variants. But it might prevent us from getting severely sick, effectively turning a nasty virus into something similar to the common cold.

Manuela Callari

Dr Manuela Callari is a Sydney-based freelance science writer who specialises in health and medical stories.

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How the immune system remembers viruses

When a virus enters the body, it is picked up by certain cells of the immune system. They transport the virus to the lymph nodes where they present its fragments, known as antigens, to CD8+ T cells responsible control of viral infections. Each of these cells carries a unique T cell receptor on the surface that can recognize certain antigens. However, only very few T cell receptors match a given viral the antigen.

To bring the infection under control and maximize the defenses against the virus, these few antigen-specific T cells start dividing rapidly and develop into effector T cells. These kill virus-infected host cells and then die off themselves once the infection is cleared. Some of these short-lived effector cells -- according to the generally accepted theory -- turn into memory T cells, which persist in the organism long term. In case the same pathogen enters the body again, memory T cells are already present and ready to fight the invader more swiftly and effectively than during the first encounter.

Memory cells and their origin

"Prevailing scientific opinion says that activated T cells first become effector cells and only then gradually develop into memory cells," says Dr. Veit Buchholz, a specialist in microbiology and working group leader at the Institute for Medical Microbiology, Immunology and Hygiene at TUM. "In our view, however, that isn't the case. It would mean that the more effector cells are formed after contact with the pathogen, the more numerous the memory cells would become." However, Buchholz and his colleagues observed a different course of events and have now published their results in the journal Nature Immunology.

"We investigated the antiviral immune responses resulting from individual activated T cells in mice and traced the lineage of the ensuing memory cells using single-cell fate mapping," reports first author Dr. Simon Grassmann. "Based on these experiments, we were able to show that certain 'T cell families' descended from individual cells form up to 1000 times more 'memory' than others. However, these long-term dominating T cell families only contributed little to the magnitude of the initial immune response, which was dominated by effector cells derived from other shorter-lived T cell families."

At the level of individual cells, it therefore became evident that development of effector and memory cells segregates at a much earlier stage than previously believed: "Already in the first week after the confrontation with the pathogen, we saw major differences in the transcriptomes of the detected T cell families," says Lorenz Mihatsch, also a first author of the study. "Normally at this time of the immune response CD8+ T cells are enriched in molecules that help to kill virus infected cells. However, we found no indication of these cytolytic molecules in the long-term dominating T cell families. Instead, they were already geared exclusively towards memory development at this early stage."

Optimization of vaccines

These results could help to improve vaccine development in the future, says Veit Buchholz: "To generate an optimal immune response through vaccination, the body needs to produce as many memory cells as possible. For that purpose, it is important to have a precise understanding of how individual T cells are programmed." Buchholz's study might also prove useful in helping to recognize sooner whether a new vaccine is effective. "To determine the long-term strength of an immune response, it could be helpful to measure the number of memory precursors within a few days of administering a vaccine," says Buchholz.

Immune T Cells May Offer Lasting Protection Against COVID-19

Caption: Scanning electron micrograph of a human T lymphocyte (T cell) from a healthy donor’s immune system. Credit: National Institute of Allergy and Infectious Diseases/NIH

Much of the study on the immune response to SARS-CoV-2, the novel coronavirus that causes COVID-19, has focused on the production of antibodies. But, in fact, immune cells known as memory T cells also play an important role in the ability of our immune systems to protect us against many viral infections, including—it now appears—COVID-19.

An intriguing new study of these memory T cells suggests they might protect some people newly infected with SARS-CoV-2 by remembering past encounters with other human coronaviruses. This might potentially explain why some people seem to fend off the virus and may be less susceptible to becoming severely ill with COVID-19.

The findings, reported in the journal Nature, come from the lab of Antonio Bertoletti at the Duke-NUS Medical School in Singapore [1]. Bertoletti is an expert in viral infections, particularly hepatitis B. But, like so many researchers around the world, his team has shifted their focus recently to help fight the COVID-19 pandemic.

Bertoletti’s team recognized that many factors could help to explain how a single virus can cause respiratory, circulatory, and other symptoms that vary widely in their nature and severity—as we’ve witnessed in this pandemic. One of those potential factors is prior immunity to other, closely related viruses.

SARS-CoV-2 belongs to a large family of coronaviruses, six of which were previously known to infect humans. Four of them are responsible for the common cold. The other two are more dangerous: SARS-CoV-1, the virus responsible for the outbreak of Severe Acute Respiratory Syndrome (SARS), which ended in 2004 and MERS-CoV, the virus that causes Middle East Respiratory Syndrome (MERS), first identified in Saudi Arabia in 2012.

All six previously known coronaviruses spark production of both antibodies and memory T cells. In addition, studies of immunity to SARS-CoV-1 have shown that T cells stick around for many years longer than acquired antibodies. So, Bertoletti’s team set out to gain a better understanding of T cell immunity against the novel coronavirus.

The researchers gathered blood samples from 36 people who’d recently recovered from mild to severe COVID-19. They focused their attention on T cells (including CD4 helper and CD8 cytotoxic, both of which can function as memory T cells). They identified T cells that respond to the SARS-CoV-2 nucleocapsid, which is a structural protein inside the virus. They also detected T cell responses to two non-structural proteins that SARS-CoV-2 needs to make additional copies of its genome and spread. The team found that all those recently recovered from COVID-19 produced T cells that recognize multiple parts of SARS-CoV-2.

Next, they looked at blood samples from 23 people who’d survived SARS. Their studies showed that those individuals still had lasting memory T cells today, 17 years after the outbreak. Those memory T cells, acquired in response to SARS-CoV-1, also recognized parts of SARS-CoV-2.

Finally, Bertoletti’s team looked for such T cells in blood samples from 37 healthy individuals with no history of either COVID-19 or SARS. To their surprise, more than half had T cells that recognize one or more of the SARS-CoV-2 proteins under study here. It’s still not clear if this acquired immunity stems from previous infection with coronaviruses that cause the common cold or perhaps from exposure to other as-yet unknown coronaviruses.

What’s clear from this study is our past experiences with coronavirus infections may have something important to tell us about COVID-19. Bertoletti’s team and others are pursuing this intriguing lead to see where it will lead—not only in explaining our varied responses to the virus, but also in designing new treatments and optimized vaccines.

[1] SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls. Le Bert N, Tan AT, Kunasegaran K, et al. Nature. 2020 July 15. [published online ahead of print]

Overview of the Immune System (National Institute of Allergy and Infectious Diseases/NIAID)

T Cells Recognize Recent SARS-CoV-2 Variants

Scanning electron micrograph of a human T lymphocyte (also called a T cell) from the immune system of a healthy donor.

Scanning electron micrograph of a human T lymphocyte (also called a T cell) from the immune system of a healthy donor.

When variants of SARS-CoV-2 (the virus that causes COVID-19) emerged in late 2020, concern arose that they might elude protective immune responses generated by prior infection or vaccination, potentially making re-infection more likely or vaccination less effective. To investigate this possibility, researchers from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and colleagues analyzed blood cell samples from 30 people who had contracted and recovered from COVID-19 prior to the emergence of virus variants. They found that one key player in the immune response to SARS-CoV-2—the CD8+ T cell—remained active against the virus.

The research team was led by NIAID’s Andrew Redd, Ph.D., and included scientists from Johns Hopkins University School of Medicine, Johns Hopkins Bloomberg School of Public Health and the immunomics-focused company, ImmunoScape.

The investigators asked whether CD8+ T cells in the blood of recovered COVID-19 patients, infected with the initial virus, could still recognize three SARS-CoV-2 variants: B.1.1.7, which was first detected in the United Kingdom B.1.351, originally found in the Republic of South Africa and B.1.1.248, first seen in Brazil. Each variant has mutations throughout the virus, and, in particular, in the region of the virus’ spike protein that it uses to attach to and enter cells. Mutations in this spike protein region could make it less recognizable to T cells and neutralizing antibodies, which are made by the immune system’s B cells following infection or vaccination.

Although details about the exact levels and composition of antibody and T-cell responses needed to achieve immunity to SARS-CoV-2 are still unknown, scientists assume that strong and broad responses from both antibodies and T cells are required to mount an effective immune response. CD8+ T cells limit infection by recognizing parts of the virus protein presented on the surface of infected cells and killing those cells.

In their study of recovered COVID-19 patients, the researchers determined that SARS-CoV-2-specific CD8+ T-cell responses remained largely intact and could recognize virtually all mutations in the variants studied. While larger studies are needed, the researchers note that their findings suggest that the T cell response in convalescent individuals, and most likely in vaccinees, are largely not affected by the mutations found in these three variants, and should offer protection against emerging variants.

Optimal immunity to SARS-Cov-2 likely requires strong multivalent T-cell responses in addition to neutralizing antibodies and other responses to protect against current SARS-CoV-2 strains and emerging variants, the authors indicate. They stress the importance of monitoring the breadth, magnitude and durability of the anti-SARS-CoV-2 T-cell responses in recovered and vaccinated individuals as part of any assessment to determine if booster vaccinations are needed.

AD Redd et al. CD8+ T cell responses in COVID-19 convalescent individuals target conserved epitopes from multiple prominent SARS-CoV-2 circulating variants. Open Forum Infectious Diseases DOI: 10.1093/ofid/ofab143 (2021).

Anthony S. Fauci, M.D., NIAID Director and Chief, Laboratory of Immunoregulation, is available to comment on this research. Dr. Andrew Redd, staff scientist in the Laboratory of Immunoregulation, is also available.

This work was supported in part by NIAID grants R01AI120938, R01AI120938S1 and R01AI128779 and by National Heart Lung and Blood Institute grant 1K23HL151826-01.

Adaptive Immunity and the Immunoglobulin Superfamily

Adaptive immunity is stimulated by exposure to infectious agents and recruits elements of the immunoglobulin superfamily.

Learning Objectives

Describe the role of immunoglobulins in the adaptive immune response, specifically in humoral immunity

Key Takeaways

Key Points

  • The concept of adaptive immunity suggests de novo generation in each individual of extremely large repertoires of diversified receptors and selective expansion of receptors that match the antigen /pathogen.
  • Adaptive immune receptors of T and B lymphoid cells belong to the immunoglobulin superfamily and are created by rearrangement of gene segments.
  • Immunoglobulins are glycoproteins in the immunoglobulin superfamily that function as antibodies.

Key Terms

  • cytokine: Any of various small regulatory proteins that regulate the cells of the immune system.

Precision of Immunoglobulin

Adaptive immunity is stimulated by exposure to infectious agents and increases in magnitude and defensive capabilities with each successive exposure to a particular microbe. The defining characteristics of adaptive immunity are specificity for distinct molecules and an ability to “remember” and respond more vigorously to repeated exposures to the same microbe.

The components of adaptive immunity are lymphocytes and their products. There are two types of adaptive immune responses: humoral immunity and cell-mediated immunity. These are driven by different elements of the immune system and function to eliminate different types of microbes. Protective immunity against a microbe may be induced by the host ‘s response to the microbe or by the transfer of antibodies or lymphocytes specific for the microbe. Antibodies or Immunoglobulins bind antigens in the recognition phase and the effector phase of humoral immunity.

The Immunoglobulin Superfamily

Immunoglobulins are produced in a membrane -bound form by B lymphocytes. These membrane molecules function as B cell receptors for antigens. The interaction of antigens with membrane antibodies on naive B cells initiates B cell activation. These activated B cells produce a soluble form of immunoglobulin that triggers effector mechanisms to eliminate antigens.

B cell activation: When a B cell encounters its triggering antigen, it gives rise to many large cells known as plasma cells. Every plasma cell is essentially a factory for producing an antibody. Each of the plasma cells manufactures millions of identical antibody molecules and pours them into the bloodstream.

These antibodies are part of a larger family called the immunoglobulin superfamily. The immunoglobulin superfamily (IgSF) is a large group of cell surface and soluble proteins that are involved in the recognition, binding, or adhesion processes of cells. Molecules are categorized as members of this superfamily based on structural features shared with immunoglobulins, which are also known as antibodies. They all possess a domain known as an immunoglobulin domain or fold. Members of the IgSF include cell surface antigen receptors, co-receptors, and co-stimulatory molecules of the immune system, molecules involved in antigen presentation to lymphocytes, cell adhesion molecules, certain cytokine receptors, and intracellular muscle proteins. They are commonly associated with roles in the immune system.

Among the methods used for studying T cells, multicolor flow cytometry is preeminent because it enables the characterization of highly complex T cell subpopulations—both functionally and phenotypically. Complementary technologies such as ELISA, ELISPOT and bead-based immunoassays also further research in the T cell area, offering flexibility to meet a range of experimental needs and multiple methods to verify results.

The following table lists important characteristics of tools and technologies to support your T cell research and help you find the ones that meet your experimental needs. Certain technologies can reveal specific information about a sample or might better meet practical needs such as the available instrumentation or sample type. In some cases, researchers can use the combined information from multiple techniques to verify results. Different approaches can paint a detailed picture of the mechanisms contributing to T cell development.

Tool/Technology Flow Cytometry: Surface Flow Cytometry: Introcellular BD ® Cytometric Bead Array (CBA) ELISPOT ELISA In Vivo Capture Assay
Molecules detected Surface Intracellular and surface Secreted or intracellular Secreted (in situ) Secreted Secreted (in vivo)
Multiparameter Yes Yes Yes No No No
Single cell/cell subset information Yes Yes No Frequencies, no subset information No No
Antigen-specific Yes Yes Yes Yes Yes Yes
Post-assay viability Yes No Yes, for secreted molecules No Yes Yes
Quantitation of protein Possible* Possible* Yes No Yes Yes
Instrumentation Flow cytometer Flow cytometer Flow cytometer ELISPOT reader Spectrophotometer Spectrophotometer

*With a standard such as BD Quantibrite&trade Beads

Bystander Effects

CTL responses

Cytotoxic T cells (CTLs) are differentiated effector T lymphocytes that specifically kill target cells bearing an appropriate antigenic complex (peptide–MHC) recognized by their T cell receptor. However, during this process, nonspecific lysis of unrelated bystander target cells can be observed in the culture. The unrelated target cells do not exhibit the appropriate antigenic complex on their surface and therefore cannot be recognized by the T cell receptor. This phenomenon can be detected in vitro using cytotoxic T cell lines of defined specificity and mixing together target cells bearing the appropriate or unrelated antigenic complex.

Antibodies fight off the new coronavirus, but what do T cells do?

Our immune systems are primed to fight off viruses. As evidence about how our bodies react to SARS-CoV-2 emerges, we look at how different immune cells work together to fend off the new coronavirus, and why T cells may play a greater role than scientists initially thought.

Share on Pinterest T cells may play a more significant role in fighting off COVID-19 than scientists previously thought.

Many people will be familiar with the concept of antibodies that our bodies generate to fight off infection.

In the battle against the new coronavirus SARS-CoV-2, scientists have widely hailed the presence of neutralizing antibodies as the holy grail of immunity to future infections.

However, antibodies do not exist in isolation. In fact, several cells in our body have to work together before antibodies, particularly neutralizing antibodies, enter the stage.

One sub-set of T cells are crucial actors in the intricate interplay that leads to antibody production. Another type of T cell kills cells that viruses have infected.

Now T cells are emerging as an additional route to immunity in the context of COVID-19.

But what are T cells, and why are they key players in the fight against the new coronavirus?

To understand what T cells do and their relationship with antibodies and short- and long-term immunity, we have to delve into the science of immunology.

T cells are a type of lymphocyte, or white blood cell. The bone marrow produces them in the form of progenitor cells, and they migrate to the thymus, hence the name T cells.

There are several types of T cells.

In a recent This Week in Virology (TWiV) podcast, Dr. Jon Yewdell , who is the Chief of the Cellular Biology Section at the Laboratory of Viral Diseases at the National Institute of Allergy and Infectious Diseases (NIAID) in Bethesda, MD, gave an overview of T cells in the context of COVID-19.

Helper T cells, which some people call CD4 T cells, or CD4 helper T cells because they carry a protein called cluster of differentiation 4 (CD4) on their cell surface, surveil our bodies for pathogens.

Dr. Yewdell explained that when a virus infects a cell, there are two ways to alert the immune system of the foreign invader.

Once a virus has internalized in a cell, it travels through a series of compartments where enzymes unpack it and chop it into small peptides. Some of these peptides get picked up by Major Histocompatibility Complex (MHC) Class II molecules.

These molecules are part of our body’s toolkit for surveillance.

The MHC Class II molecules then circle back to the cell surface and present the viral peptide to passing cells. These peptides can activate CD4 helper T cells, which, in turn, play a crucial role. They allow B cells, another type of white blood cell and professional antibody producers, to make specific immunoglobulin (Ig) G antibodies to the viral peptide.

In response to this interaction with CD4 T helper cells, B cells then mature into either plasma cells or memory B cells. Plasma cells continue to make antibodies for several weeks, after which they move into the bone marrow. Here, they remain to provide long-term protection.

Memory B cells remain in the circulation or take up residence at strategic sites, as part of the body’s surveillance system. If our body contracts the same virus again, our memory B cells will recognize the viral antigen, process it, and re-present the viral antigen to a CD4 helper T cell.

While the CD4 helper T cells recognize antigens presented by MHC Class II molecules, cytotoxic T cells, or CD8 T cells or CD8 killer T cells, react to peptides presented by MHC Class I molecules.

When a virus infects a cell, it hijacks the cell’s machinery to make viral proteins. But some of the peptides made during this process are diverted to MHC Class I molecules, which carry them to the cell surface and present them to other cells.

This allows a cell to signal that a virus has infected it. CD8 T cells find and kill infected cells, a key mechanism in getting rid of a viral infection.

As many viruses can replicate very quickly, this process needs to be fast to stop the virus from spreading. With the help of MHC Class I molecules presenting viral peptides on the cell surface, CD8 T cells can recognize influenza-infected cells within around 1.5 hours.

CD8 T cells can turn into memory CD8 T cells , which provide fast and long-lasting responses, should the same pathogen rear its ugly head again.

In the context of COVID-19, both CD4 helper T cells and CD8 T cells have important roles to play.

In a recent article in Nature Reviews Immunology , researchers from the Institute for Immunology at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia, PA, summarized what scientists know about T cells and COVID-19 to date.

They indicate that CD8 T cell responses in people with severe COVID-19 may not be as effective as in those with a mild form of the disease. Specifically, there may be fewer CD8 T cells, and those that are present may be unable to turn into memory CD8 T cells.

They do, however, point out that not all study results fit into this narrative. In some cases, researchers saw excessive CD8 T cell responses in COVID-19 patients.

For CD4 T helper cells, the data suggest a similar pattern of potential dysregulation or dysfunction in normal responses.

“Most, although not all, patients who are hospitalized seem to mount both CD8+ and CD4+ T cell responses, and evidence points to possible suboptimal, excessive or otherwise inappropriate T cell responses associated with severe disease.”

— Zeyu Chen and E. John Wherry

“In fact, multiple distinct patterns of T cell response may exist in different patients, which suggests the possibility of distinct clinical approaches tailored to the particular immunotype of a specific patient,” they continue.

In many cases, scientists perform antibody tests to determine whether a person has developed an immune response to a viral infection.

This is different from a diagnostic test, which looks for viral genetic material to determine if a person currently has an infection.

Antibody tests are relatively straightforward. A recent, large-scale study in Spain used a combination of finger-prick testing and laboratory tests to establish how many people in the country had antibodies to SARS-CoV-2.

However, it is not so easy to test a person’s T cell response.

In a recent study comparing T cell responses between people who had recovered from COVID-19 and samples from people taken before the pandemic, scientists exposed T cell precursors from blood to viral peptides to see if this elicited CD4 helper T cell or CD8 T cell responses.

They then utilized specialist equipment to differentiate between the different types of cells that the precursors developed into.

As calls for more straightforward and speedier ways of testing whether people currently have a SARS-CoV-2 infection are gaining traction, scientists are also developing new ways of testing how our T cells respond to the new coronavirus.

Medical News Today recently spoke to James Hindley, Ph.D., from Indoor Biotechnologies, who is working on a simpler T cell test that scientists can use in routine laboratory settings.

“At first, we believe the primary use of this test will be for vaccine development, in order to determine whether a T cell response to the vaccine has been generated and whether that is adequate enough to be protective from infection,” Dr. Hindley explained.

He also foresees that public health bodies will be able to use the test to screen T cell responses to SARS-CoV-2. Together with antibody tests, this may allow them to establish the level of immunity in the population.

Scientists will need more data to elucidate how T cell and B cell responses fit into both the pathology and immunity to SARS-CoV-2 infection longer-term.

As the scientific community responds to the needs laid bare by the pandemic, new and innovative testing methods and large-scale collaborative studies will hopefully provide some of these answers.

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.


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