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15.4J: Cell-Mediated Immunity - Biology

15.4J: Cell-Mediated Immunity - Biology


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The human body can respond to antigen in many different ways. These fall into two major categories:

  • antibody-mediated immunity. Antibodies — dissolved in blood, lymph, and other body fluids — bind the antigen and trigger a response to it. (This form of immunity is also called humoral immunity.)
  • cell-mediated immunity (CMI). T cells (lymphocytes) bind to the surface of other cells that display the antigen and trigger a response. The response may involve
    • other lymphocytes
    • any of the other white blood cells (leukocytes)

Examples of Cell-Mediated Immunity

Delayed-Type Hypersensitivity (DTH): the tuberculin test

Many states in the United States require that professors and teachers (among others) be checked periodically for tuberculosis. This chronic disease, caused by Mycobacterium tuberculosis, evokes an immune response that, unfortunately, does not cure the patient, but does provide an inexpensive test for the disease called the tuberculin test (or Mantoux test). A tiny amount of protein, extracted from the bacteria, is injected into the skin. If the subject is currently infected, or has ever been infected, with the bacteria, a positive test results. In 24 hours or so, a hard, red nodule develops at the site of the injection. This nodule is densely packed with lymphocytes and macrophages.

In Europe, most people produce a positive tuberculin reaction, not because they have had the infection, but because earlier they had been vaccinated against tuberculosis with a preparation of a related (but harmless) bacterium called BCG.

The response to tuberculin is called "delayed" because of the time it takes to occur (in contrast to the "immediate" responses characteristic of many antibody-mediated sensitivities like an allergic response to a bee sting).

DTH is a cell-mediated response (in fact, anti-tuberculin antibodies are rarely found in tuberculin-positive people). The T cells responsible for DTH are members of the CD4+ subset.

Contact Sensitivity

Many people develop rashes on their skin following contact with certain chemicals. Nickel, certain dyes, and the active ingredient of the poison ivy plant are common examples. The response takes some 24 hours to occur, and like DTH, is triggered by CD4+ T cells. The actual antigen is probably created by the binding of the chemical to proteins in the skin. After the antigen is engulfed by dendritic cells in the skin, they migrate to nearby lymph nodes where they present fragments of the antigen to CD4+ T cells. The activated T cells migrate from the lymph nodes to the skin to elicit the inflammatory response.

Killing intracellular parasites

Some human pathogens avoid exposure to antibodies by taking up residence within cells. These include all viruses (discussed in the next section), and some bacteria such as

  • the bacterium that causes Legionnaires's disease
  • Listeria monocytogenes, that humans sometimes acquire from contaminated food and even some protozoans.

These microorganisms are engulfed by phagocytic cells, like macrophages, but evade the normal intracellular mechanisms that should destroy them. However, the macrophages can present fragments of antigens derived from these parasites. These are displayed in the class II histocompatibility molecules of the macrophages. CD4+ T cells responding to these epitopes release lymphokines that stimulate the macrophages sufficiently that they can now begin to destroy the organisms.


Cell-Mediated Immunity

Many states in the United States require that professors and teachers (among others) be checked periodically for tuberculosis. This chronic disease, caused by Mycobacterium tuberculosis, evokes an immune response that, unfortunately, does not cure the patient, but does provide an inexpensive test for the disease called the tuberculin test (or Mantoux test).

A tiny amount of protein, extracted from the bacteria, is injected into the skin. If the subject is currently infected, or has ever been infected, with the bacteria, a positive test results. In 24 hours or so, a hard, red nodule develops at the site of the injection. This nodule is densely packed with lymphocytes and macrophages.

(In Europe, most people produce a positive tuberculin reaction, not because they have had the infection, but because earlier they had been vaccinated against tuberculosis with a preparation of a related (but harmless) bacterium called BCG.)

The response to tuberculin is called "delayed" because of the time it takes to occur (in contrast to the "immediate" responses characteristic of many antibody-mediated sensitivities like an allergic response to a bee sting).

DTH is a cell-mediated response (in fact, anti-tuberculin antibodies are rarely found in tuberculin-positive people). The T cells responsible for DTH are members of the CD4 + subset.

Contact Sensitivity

Many people develop rashes on their skin following contact with certain chemicals. Nickel, certain dyes, and the active ingredient of the poison ivy plant are common examples.

The response takes some 24 hours to occur, and like DTH, is triggered by CD4 + T cells.

The actual antigen is probably created by the binding of the chemical to proteins in the skin. After the antigen is engulfed by dendritic cells in the skin, they migrate to nearby lymph nodes where they present fragments of the antigen to CD4 + T cells .

The activated T cells migrate from the lymph nodes to the skin (link to a description of how they do this) to elicit the inflammatory response.

Killing intracellular parasites

Some human pathogens avoid exposure to antibodies by taking up residence within cells. These include all viruses (discussed in the next section), and some bacteria such as

  • the bacterium that causes Legionnaires's disease
  • Listeria monocytogenes, that humans sometimes acquire from contaminated food, and

These microorganisms are engulfed by phagocytic cells, like macrophages, but evade the normal intracellular mechanisms that should destroy them.

However, the macrophages can present fragments of antigens derived from these parasites. These are displayed in the class II histocompatibility molecules of the macrophages. CD4 + T cells responding to these epitopes release lymphokines that stimulate the macrophages sufficiently that they can now begin to destroy the organisms.

Anti-Viral Immunity

Any cell in the body is a potential target for one kind of virus or another. However, all cells express class I histocompatibility molecules at their surface. These can display antigenic fragments of viral components. CD8 + T cells that can bind to these epitopes can then destroy the cell (often before it can release a fresh crop of viruses to spread the infection).

Graft Rejection

Grafts of a kidney, heart, lung, liver, etc. from one human to another always (unless donated by an identical twin) are seen by the recipient's immune system as antigenic and elicit an immune response. If unchecked, this response will eventually lead to destruction of the graft. Both CD4 + and CD8 + T cells participate in graft rejection. They are responding to differences between donor and host of their class II and class I histocompatibility molecules (respectively).

Nude mice are homozygous for a gene that is essential for the development of a thymus. Lacking a thymus they cannot produce T cells and hence are unable to reject grafts. Link to a view of nude mice carrying various skin grafts without rejecting them.

Graft-versus-host disease

Grafts of bone marrow are used to provide, or restore, a source of blood cells for the recipient.

For example, a number of different cancers are treated so vigorously &mdash by radiation and cytotoxic chemicals &mdash that the patient's bone marrow is destroyed in the process. Grafts of bone marrow can restore the patient. Sometimes the patient's own bone marrow &mdash stored earlier and, if needed, treated to remove any cancer cells &mdash is used.

Sometimes the marrow must come from another person. In this case, there is no danger of rejecting the graft because the recipient has no functioning immune system. However, if there are any histocompatibility differences between donor and recipient (and there always are some, unless the patient's own marrow is used or that of an identical twin), then the T cells of the donor will mount an immune response against the tissues of the recipient. Fortunately, graft-versus-host disease can usually be controlled with immunosuppressive drugs.


Cell Mediated & Humoral Immune Response (With Diagram) | Immunology | Biology

An immune response is a two-way assault on a pathogen – the cell mediated immune response and the humoral immune response.

Cell Mediated Immune Response:

Cell mediated immune response is carried out by the T-cells or T lymphocytes (Fig. 11). So, it is also called T-cell immunity. This type of immune response is to defend against pathogens that may invade host cells. The surface of the T-cell has receptor molecule that can bind with antigens. These receptor molecules are made of a variable unit similar to the variable portion of the humoral antibody. A single T-cell has about 100,000 receptor sites.

When an antigen enters the body, the macrophages first attack the antigen and fragment it into pieces. It then presents a piece of antigen to the T-helper cells. The T helper cells recognize the antigen and trigger off a series of cell mediated response. A clone of T-lymphocytes is first formed after being activated by the T-helper cells. There are different kinds of T-cells, which are morphologically similar but differ functionally.

The actions of the different types of T-cell are summarised below:

a. Helper cells react by producing small peptide molecules called lymphokines. The lymphokines promote proliferation of more T-cells, stimulate B cells to produce antibodies and also help in accumulating macrophages in the inflamed tissues and by promoting phagocytosis.

b. Cytotoxic cells or Killer cells kill cells infected by viruses, cancerous cells and transplants.

c. Suppressor cells, the third type of T-cells produce lymphokines that suppress the action of the phagocytes and the different types of WBC cells. They play an important role in immunotolerance.

d. Some of the cells remain as the memory cells that get lodged in the lymphoid tissue throughout the body. These on subsequent exposure to the same antigen can cause an immune response more rapidly than the first exposure.

Humoral Immune Response:

Humoral immune response is also called B-cell mediated immunity because B-lymphocytes are involved in this response. Humoral immune response is to defend the body against pathogens that may invade body fluids or humor. B cells are antigen specific.

During immune response, B cells, specific for the antigen, enlarge to become lymphoblasts that further differentiate to form plasma cells. The mature plasma cells produce gamma globulins or immunoglobulins called antibodies at a rapid rate of about 2000 molecules per second for each plasma cell. The antibodies secreted into the lymph eventually enter the blood.

The antibody molecule is the basic functional unit of this type of immune response. So this immune response is also called antibody-mediated immune response. The flow chart summarizes the various steps involved in the humoral response.


Biological safety concepts of genetically modified live bacterial vaccines

Live vaccines possess the advantage of having access to induce cell-mediated and antibody-mediated immunity thus in certain cases they are able to prevent infection, and not only disease. Furthermore, live vaccines, particularly bacterial live vaccines, are relatively cheap to produce and easy to apply. Hence they are suitable to immunize large communities or herds. The induction of both cell-mediated immunity as well as antibody-mediated immunity, which is particularly beneficial in inducing mucosal immune responses, is obtained by the vaccine-strain's ability to colonize and multiply in the host without causing disease. For this reason, live vaccines require attenuation of virulence of the bacterium to which immunity must be induced. Traditionally attenuation was achieved simply by multiple passages of the microorganism on growth medium, in animals, eggs or cell cultures or by chemical or physical mutagenesis, which resulted in random mutations that lead to attenuation. In contrast, novel molecular methods enable the development of genetically modified organisms (GMOs) targeted to specific genes that are particularly suited to induce attenuation or to reduce undesirable effects in the tissue in which the vaccine strains can multiply and survive. Since live vaccine strains (attenuated by natural selection or genetic engineering) are potentially released into the environment by the vaccinees, safety issues concerning the medical as well as environmental aspects must be considered. These involve (i) changes in cell, tissue and host tropism, (ii) virulence of the carrier through the incorporation of foreign genes, (iii) reversion to virulence by acquisition of complementation genes, (iv) exchange of genetic information with other vaccine or wild-type strains of the carrier organism and (v) spread of undesired genes such as antibiotic resistance genes. Before live vaccines are applied, the safety issues must be thoroughly evaluated case-by-case. Safety assessment includes knowledge of the precise function and genetic location of the genes to be mutated, their genetic stability, potential reversion mechanisms, possible recombination events with dormant genes, gene transfer to other organisms as well as gene acquisition from other organisms by phage transduction, transposition or plasmid transfer and cis- or trans-complementation. For this, GMOs that are constructed with modern techniques of genetic engineering display a significant advantage over random mutagenesis derived live organisms. The selection of suitable GMO candidate strains can be made under in vitro conditions using basic knowledge on molecular mechanisms of pathogenicity of the corresponding bacterial species rather than by in vivo testing of large numbers of random mutants. This leads to a more targeted safety testing on volunteers and to a reduction in the use of animal experimentation.


Nutrition and immunology: from the clinic to cellular biology and back again

Diet and immunity have been known to be linked to each other for centuries. In the last 30 years systematic studies have confirmed that nutrient deficiencies impair immune response and lead to frequent severe infections resulting in increased mortality, especially in children. Protein-energy malnutrition results in reduced number and functions of T-cells, phagocytic cells and secretory immunoglobulin A antibody response. In addition, levels of many complement components are reduced. Similar findings have been reported for moderate deficiencies of individual nutrients such as trace minerals and vitamins, particularly Zn, Fe, Se, vitamins A, B6, C and E. For example, Zn deficiency is associated with profound impairment of cell-mediated immunity such as lymphocyte stimulation response, decreased CD4+:CD8+ cells, and decreased chemotaxis of phagocytes. In addition, the level of thymulin, which is a Zn-dependent hormone, is markedly decreased. The use of nutrient supplements, singly or in combination, stimulates immune response and may result in fewer infections, particularly in the elderly, low-birth-weight infants and malnourished critically-ill patients in hospitals. The interactions between nutrition and the immune system are of clinical, practical and public health importance.


What is Cell Mediated Immunity

Cell mediated immunity is the immunity mediated by antigen-specific T cells. T cells are produced in the bone marrow and are matured in the thymus. After they enter the bloodstream, T cells occur can be found in the blood as well as in lymphoid tissue. The antigens should be presented on the surface of the antigen-presenting cells (APCs) along with the major histocompatibility complexes (MHC). Once T cells encounter an antigen, they proliferate and differentiate into armed effector cells. The cytotoxic T cells destroy the infected cells by inducing apoptosis. T helper cells stimulate plasma B cells to produce antibodies.

Figure 2: Cell Mediated Immunity

The IgG and IgM are the main two types of antibodies produced by T helper cells in response to plasma B cells. The memory T cells are differentiated T cells, but their action requires the activation by the specific antigen. The major characteristic feature of the cell mediated immunity is that it destroys intracellular pathogens. The cell mediated immunity is shown in figure 2.


Cell-mediated immunity

cell-mediated immunity Immune reaction directed against body cells that have been infected by viruses and bacteria controlled by T cells.

cell-mediated immunity
The type of immunity that functions in defense against fungi, protists, bacteria, and viruses inside host cells and against tissue transplants, with highly specialized cells that circulate in the blood and lymphoid tissue.
cell membrane .

Cell-Mediated Immunity
Unlike B cells, T lymphocytes are unable to recognize pathogens without assistance. Instead, dendritic cells and macrophages first engulf and digest pathogens into hundreds or thousands of antigens.

(CMI) Immunity in which antigen is bound to receptor sites on the surface of sensitized T lymphocytes that have been produced in response to prior immunizing experience with that antigen and in which manifestation is through macrophage response with no intervention of antibody.

: Immunity resulting from destruction of foreign organisms and infected cells by the active action of T-lymphocytes on them. It can be acquired by individuals by the transfer of cells.

, stimulated T H cells activate T C cells. All cells of the body produce surface proteins called class I MHC proteins. If the cell is abnormal (cancerous or infected with a virus), the abnormal antigen is displayed with the class I MHC protein.

, activation and clonal selection of cytotoxic T lymphocytes allows these cells to directly destroy certain target cells, including "nonself" cancer and transplant cells.
The humoral and cell-mediated immune responses are linked by cell-signaling interactions, especially via helper T cells.

(Antibody)(Cytotoxicity)
Some of these responses are specific, others are non-specific. This page will introduce host defense mechanisms by defining some commonly used terms and describing the specific cells and tissues involved in these immune responses.

". Annual Review of Immunology 16 (1): 111-35. doi:10.1146/annurev.immunol.16.1.111. PMID 9597126.
^ Girardi M (Jan 2006). "Immunosurveillance and immunoregulation by gammadelta T cells". The Journal of Investigative Dermatology 126 (1): 25-31. doi:10.1038/sj.jid.

What's the difference between humoral-mediated and

?
As part of the adaptive-or specific-immune system, we have cells that are called B-cells. They produce antibodies that are released by these cells and circulate in the blood, or throughout the body.

A second defence of vertebrates against viruses is called

and involves immune cells known as T cells.

IL-10 can enhance humoral immunity by inhibiting

to resist HF. Thus, IL-10 is considered to be a candidate for the management of HF, [12]. Serum level of pro-inflammatory cytokines of tumor necrosis factor &alpha (TNF-&alpha) are found to be elevated in experimental models of HF [15].

A type of lymphocyte responsible for

that differentiates under the influence of the thymus.
taiga
(ty-guh)
The coniferous or boreal forest biome, characterized by considerable snow, harsh winters, short summers, and evergreen trees.

The spleen is primarily associated with RBC turnover, but it also plays a role in the lymphatic system, clearing bacteria and other pathogens that have been coated with antibodies.

from T-cells is also seen in the spleen.
Functions of the Lymphatic System .


15.4J: Cell-Mediated Immunity - Biology

Cell-mediated immunity is an immune response that does not involve antibodies or complement but rather involves the activation of macrophages, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity.
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Aspects of the topic cell-mediated-immunity are discussed in the following places at Britannica. Assorted References function of T cells ( in blood (biochemistry): Lymphocytes . lymphocytes (or T cells), are involved in regulating the antibody-forming function of B lymphocytes as well as in directly attacking foreign antigens. T lymphocytes participate in.
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. Immunity. Cell-mediated Immunity. Humoral . but sensitized in the thymus and constitute the basis of cell-mediated immunity. . Cell-mediated immunity .
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Cell-mediated immunity summary with 11 pages of encyclopedia entries, essays, summaries, research information, and more. . Immunity, Cell Mediated Summary .
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Cell-Mediated Immunity: Review the latest approaches to developing an effective HCV vaccine. . Humoral Immunity. Cell-Mediated Immunity. Obstacles In .
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(a) T cells mediate cell-mediated immunity . (27) Cell-mediated immunity . (b) Cell-mediated immunity is particularly active against virus-infected cells, .
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Cytotoxic T cell mediated immunity. Cyotoxic T lymphocyte. Giant cells. Inclusion bodies . The effect of cell-mediated immunity is infected cell death. .
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. is the aspect of immunity that is mediated by secreted antibodies (as opposed . cell-mediated immunity, which involves T lymphocytes) produced in the cells of .
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cell-mediated immunity (CMI) . Examples of Cell-Mediated Immunity. Delayed-Type Hypersensitivity (DTH): the tuberculin test .
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Cell Mediated and Humoral Immunity . are produced primarily by B Cell lymphocytes. The body's cell mediated immunity involved T cells, macrophages, and other .
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Neopterin as a marker for activated cell-mediated immunity: application in HIV infection . is closely correlated with activation of cell-mediated immunity. .
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Introduction: Cell-Mediated Basic Immunity. Hepatitis United . Cell Mediated Immunity employs an army of cells to attack and kill invaders. .
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Decrease In Cell-Mediated Immunity –A Marker For Allostatic Load Effects on Immune Function . and chronic stress suppresses, cell-mediated immunity in vivo. .
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Regulatory T Cells

Regulatory T cells are a subset of T cells which modulate the immune system and keep immune reactions in check.

Learning Objectives

Describe the function and types of regulatory T cells

Key Takeaways

Key Points

  • Regulatory T cells (Tregs) are critical to the maintenance of immune cell homeostasis as evidenced by the consequences of genetic or physical ablation of the Treg population.
  • Tregs are classified into natural or induced Tregs natural Tregs are CD4+CD25+ T-cells which develop, and emigrate from the thymus to perform their key role in immune homeostasis.
  • Adaptive Tregs are non-regulatory CD4+ T-cells which acquire CD25 (IL-2R alpha) expression outside of the thymus and are typically induced by inflammation and disease processes, such as autoimmunity and cancer.

Key Terms

  • autoimmunity: The condition where one’s immune system attacks one’s own tissues, i.e., an autoimmune disorder.

Regulatory T cells are a component of the immune system that suppress immune responses of other cells. This is an important “self-check” built into the immune system to prevent excessive reactions and chronic inflammation. Regulatory T cells come in many forms, with the most well-understood being those that express CD4, CD25, and Foxp3. These cells are also called CD4 + CD25 + regulatory T cells, or Tregs. These cells are involved in shutting down immune responses after they have successfully eliminated invading organisms, and also in preventing autoimmunity.

CD25 is a component of the IL2 receptor: Interleukin 2 receptor is composed of three subunits (alpha, beta, and gamma). CD25 constitutes the alpha chain of the IL2 receptor.

CD4 + Foxp3 + regulatory T cells have been called “naturally-occurring” regulatory T cells, to distinguish them from “suppressor” T cell populations that are generated in vitro. Additional suppressor T cell populations include Tr1, Th3, CD8 + CD28 – , and Qa-1 restricted T cells. The contribution of these populations to self- tolerance and immune homeostasis is less well defined. FOXP3 can be used as a good marker for CD4+CD25+ T cells as well as recent studies showing evidence for FOXP3 in CD4+CD25- T cells.

An additional regulatory T cell subset, induced regulatory T cells, are also needed for tolerance and suppression. Induced Regulatory T (iTreg) cells (CD4 + CD25 + Foxp3 + ) are suppressive cells involved in tolerance. iTreg cells have been shown to suppress T cell proliferation and experimental autoimmune diseases. iTreg cells develop from mature CD4 + conventional T cells outside of the thymus: a defining distinction between natural regulatory T (nTreg) cells and iTreg cells. Though iTreg and nTreg cells share a similar function iTreg cells have recently been shown to be an essential non-redundant regulatory subset that supplements nTreg cells, in part by expanding TCR diversity within regulatory responses. Acute depletion of the iTreg cell pool in mouse models has resulted in inflammation and weight loss. The contribution of nTreg cells versus iTreg cells in maintaining tolerance is unknown, but both are important. Epigenetic differences have been observed between nTreg and iTreg cells, with the former having more stable Foxp3 expression and wider demethylation.


Content: Humoral Vs Cell-Mediated Immunity

Comparison Chart

Definition of Humoral Immunity

Humoral immune response or antibody-mediated response is associated with the B cells, where the role of these cells (B cells) is to identify the antigens or any foreign particle that are present in the circulation in blood or lymph. This immune response is also assisted with helper T cells which along with the B cells get differentiated into plasma B cells that can produce antibodies.

As soon as B cells produce antibodies, they will bind to an antigen neutralize them and causes phagocytosis or cell lysis (destruction of the cells). The antigen is the foreign particle, which is usually a carbohydrate or a protein that triggers an immune response, but above that our body has tremendous capability to identify the antigens.

Any kind exposure of antigens leads to the development of secondary immunological response which increases the level of the immune response. The immunoglobulins or antibodies mediate the humoral immunity, these are a particular group of proteins produced by the B-lymphocytes.

This following points can explain the eventual process:

  • Antigens triggers to the body.
  • Antigens bind to the B cells present in the blood circulation.
  • Helper T cells or Interleukins assist the B cells and initiate B cell proliferation which activates plasma B cells.
  • Plasma cells carry antibodies which are antigen-specific and has specific binding receptors of the activated B cells.
  • These antibodies travel throughout the body and bind to the antigens.
  • The B cells after destroying the antigens, produce memory cells which in turn provide future immunity when the same antigen triggers the body again.

Definition of Cell-Mediated Immunity

T lymphocytes assist the Cell-mediated immunity or cellular immunity. In this type, cytokines have released that help to activate the T cells which further destroys the infected cell. Likewise the B cells, T cells originate in bone marrow but matures in the thymus and later gets circulate in the bloodstream and lymphoid tissue.

The antigen present on the surface of the antigen-presenting cells (APCs) with the abnormal Major Histocompatibility Complex (MHC) proteins. Abnormal or aberrant MHC molecules are formed from the antigens which have been destroyed or broken down or from any infected virus (exogenous antigens) or the from tumour cells that are actively producing foreign proteins (endogenous antigens).

Now helper T-cells release the cytokines, that will activate the T cells, which will recognize the aberrant MHC-antigen complex and will bind to it and differentiate into cytotoxic T cell. After this cell will undergo lysis (cell destruction).

This following points can explain the eventual process:

  • Antigen-presenting cells (APCs) will display the antigens present on its surface and binds to T cells.
  • Interleukins (secreted by helper T cells) facilitates the activation of T cells.
  • Along with the MHC-I and the endogenous antigens, the T cells proliferate and produce the cytotoxic T cells.
  • The T cells destroy the infected cells exhibiting antigens.
  • In case of exogenous antigens and MHC-II displayed on the plasma membrane together, the T cells trigger to proliferate helper T cells which release interleukins and cytokines and also arouse the B cells to produce antibodies against them. This process is also supported by the natural killer cells (NK) and macrophages, which destroys the antigens.

Difference Between Humoral and Cell Mediated Immunity

Definition of Humoral and Cell Mediated Immunity

Humoral Immunity: The aspect of immunity, mediated by macromolecules found in the extracellular body fluids is called humoral immunity.

Cell Mediated Immunity: The aspect of immunity that identifies and destroys infected cells is called cell mediated immunity.

Pathogens

Humoral Immunity: The humoral immunity protects against extracellular pathogens.

Cell Mediated Immunity: The cell mediated immunity protects against intracellular pathogens.

Main cells

Humoral Immunity: The main cells, involved in the humoral immunity are the B-cells. Thеse cells are generated and mature in the bone marrow.

Cell Mediated Immunity: The main cells, involved in the cell mediated immunity are the T-cells. Thеse cells are generated in the bone marrow and complete their development in the thymus.

Activation

Humoral Immunity: The end result of the activation is the differentiation of plasma B-cells, secreting antibodies.

Cell Mediated Immunity: The end result of the activation is the secretion of cytokines.



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