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16.8: The Immune System - Biology

16.8: The Immune System - Biology


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Immunology is a full semester course at most universities, so this section will only touch on a few basic concepts that should be easily accessible to the student who has nearly completed the cell biology course. At its core, immunology is about adaptation. That is, since an animal has no preconception of the various potential infections it may be subject to, it must have a system in place that is flexible enough to deal with almost anything that comes along. Obviously, the systems are not perfect, but considering the wide range of pathogens, immune systems are remarkably efficient. In humans, there are two types of immune response to infection: the innate response, which is relatively nonspecific, and the adaptive, or acquired, response, which has more specificity.

The innate immune responses are common to all animals, and act on large classes of pathogens. For example, Toll-like receptors on phagocytes recognize a variety of bacterial surface molecules such as the flagellin specific to bacterial flagella, or the peptidoglycan components of bacterial cell walls. When these receptors are activated, the phagocyte goes into action, enveloping the offending bacteria or virus, and breaking it down. This depends on recognizing the external surface, so bacteria or viruses that do not have a recognizable molecule on their surface are able to escape this particular line of defense.

Defensins, which are found on a variety of surfaces (skin, cornea, gut) as well as in circulation, are small (18-45 amino acids) cysteine-rich cationic proteins that bind to a variety of pathogenic viruses, bacteria, and fungi. It is unclear how they may work against viruses, other than perhaps attacking infected host cells, but against bacteria and fungi the mode of operation is generally to bind to the cell membrane and form a pore that allows ions and other small molecules to ow out killing the pathogen. Complement, a group of proteins (~20) circulating in the blood, can act similarly against pathogenic cells.

Finally, natural killer (NK) cells, lymphocytes that target any cell that does not carry cell surface proteins that are normally found on cells from the animal, can kill not only attacking cells, but virally infected cells that have stopped producing their normal proteins (including the recognition protein) because they are busy producing viral proteins. NK cells can even be effective against some cancer cells if they have downregulated cell surface protein expression as part of their de-differentiation and de-adhesion.

The adaptive immune system, which is only found in vertebrates, is what most people think of when the human immune system is mentioned. We and other vertebrates also have an innate immune system, but all the molecules and cells that normally come to mind — antibodies, T-cells, B-cells — are part of the adaptive immune response. There are two components to the adaptive response, a humoral response, in which proteins (antibodies) floating in the blood bind to the infectious agent and prevent if from binding to cells or targeting it for the cellular response, which is mediated by T cells that can specifically recognize and kill the targeted pathogen.

Antibodies

Front and center in the adaptive immune response are antibodies. These proteins may be either secreted by or attached to the surface of B cells, the lymphocytes that differentiate either in bone marrow (adult) or liver (fetus), as opposed to those called T cells, which differentiate in the thymus gland. Incidentally, if you see sweetbreads on a menu, that would be thymus. Yum. You can take that seriously or sarcastically depending on how you think my tastes run.

Back to the antibodies. The different types of antibodies, IgA, IgD, IgE, IgG, and IgM, are all based on the IgG structure (Figure (PageIndex{18})), which is roughly Y-shaped, and composed of two heavy chains and two light chains. These chains have disulfide bond-stabilized loops (recall the Ig-like loops in the cell adhesion molecules a few chapters back?), and the combination of the distal light chain loop and distal heavy chain loop make the antigen binding site. The antigen is defined as the molecule, or more specifically the part of a molecule that is recognized by the particular antibody. Since the antibody is meant to mediate highly specific recognition of a wide variety of invading pathogens, there must be a way to create at least as many different antibodies. This is made possible by the process of DNA rearrangement. This mechanism is also used to generate diversity in T-cell receptors, which are quite different structurally, but also need to be available with an extremely wide variety of specific binding sites.


The Immune System

This interactive module introduces the anatomy of the immune system and walks through the timeline of a typical immune response.

The timeline includes the differences between the first time a pathogen is encountered versus subsequent infections, including an explanation of how vaccines work. Different tabs, videos, images, questions, and a detailed glossary of terms allow this resource to be explored at varying levels of depth depending on the class. Refer to the “Educator Resources” tab in the Click & Learn for implementation suggestions.

The glossary and illustrations in the Click & Learn are also provided as slide decks you may make copies of these slides and adapt them to your classroom.

The “Resource Google Folder” link directs to a Google Drive folder of resource documents in the Google Docs format. Not all downloadable documents for the resource may be available in this format. The Google Drive folder is set as “View Only” to save a copy of a document in this folder to your Google Drive, open that document, then select File → “Make a copy.” These documents can be copied, modified, and distributed online following the Terms of Use listed in the “Details” section below, including crediting BioInteractive.


16.8: The Immune System - Biology

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This text is based on Openstax Biology for AP Courses, Senior Contributing Authors Julianne Zedalis, The Bishop's School in La Jolla, CA, John Eggebrecht, Cornell University Contributing Authors Yael Avissar, Rhode Island College, Jung Choi, Georgia Institute of Technology, Jean DeSaix, University of North Carolina at Chapel Hill, Vladimir Jurukovski, Suffolk County Community College, Connie Rye, East Mississippi Community College, Robert Wise, University of Wisconsin, Oshkosh

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 Unported License, with no additional restrictions


Intermittent Fasting Boosts Your Immune System

Our ancient ancestors grew up in a world of stress and scarcity. Food was often not available and intermittent fasting was common. This form of life left a genetic blueprint with key information pertaining to our health and wellbeing. Intermittent fasting reduces free radical damage, regulates inflammatory conditions in the body and starves off cancer cell formation.

In nature, when animals get sick they stop eating and instead focus on resting. This is a primal instinct to reduce stress on their internal system so there body can fight off infection. This natural mechanism allows the animal to concentrate all their internal energy systems towards immunity. Humans are the only species that often look for more food during times of illness.

Energy Conservation in the Body:

The body has a certain amount of available energy that it diverts into important function such as digestion, physical movement (kinetics), immunity, cognition, etc. The continual need to digest food diverts energy away from these other factors while fasting conserves energy for use with these other systems. In fact, the digestive process diverts huge amounts of blood and is considered energy expensive.

When we eat food the immune system gets activated to increase inflammatory conditions to ward off any unwanted microorganisms within the food. This happens whether the food is raw or cooked as nothing is truly sterile. When the immune system activates in order to attack newly ingested pathogens it is using up its energy reserves that could be used for other activities. Fasting frees these white blood cells up to destroy dormant infections and other problematic areas.

Fasting Increases Immune Regulation

The practice of fasting allows the body to put more energy and focus into the process of effective immune regulation. Fasting while drinking water and cleansing beverages flushes out the digestive system and reduces the number of natural microorganisms in the gut. The microorganism count is typically regulated by the immune system. So this allows the immune system to divert energy to other more important areas.

Intermittent fasting is a terrific regulator of the immune system as it controls the amount of inflammatory cytokines that are released in the body. Two major cytokines Interleukin-6 and Tumor Necrosis Factor Alpha promote an inflammatory response in the body. Studies have shown that fasting reduces the release of these inflammatory mediators (1, 2, 3). The immune system modulation that intermittent fasting provides may also be helpful if you have moderate to severe allergies (4).

Autophagy to Protect the Body:

Fasting also stimulates the process of autophagy, where the body breaks down old, damaged cells and abnormally developing cells to recycle for energy. The process of autophagy is part of the innate immune system and utilizes pattern recognition receptors to identify viral cell invaders.

Intermittent fasting stimulates autophagy processes which restrict viral infections and the replication of intracellular parasites. This catabolic process helps the body rid itself of intracellar pathogens as well as abnormal cancer cell development. It is also important in protecting the brain and tissue cells from abnormal growths, toxicity and chronic inflammation (5).

Intermittent Fasting and Auto-Immunity

Individuals with auto-immune diseases such as systemic lupus, rheumatoid arthritis, colitis and Crohn&rsquos disease have seen a tremendous improvement in symptoms with the incorporation of intermittent fasting (6). This process reduces the hyper inflammatory processes these individuals undergo and allow for more normalized immune function. You can read more about how fasting improves autoimmune conditions in this article.

Cancer cells are known to have anywhere from ten to seventy times more insulin receptors than normal cells and depend upon anaerobic metabolism of sugar for fuel. Intermittent fasting starves cancer cells and leaves them vulnerable to free radical damage and ultimate destruction (7, 8). You can read about the best strategies for intermittent fasting in this article.


Β2→1-Fructans Modulate the Immune System In Vivo in a Microbiota-Dependent and -Independent Fashion

It has been shown in vitro that only specific dietary fibers contribute to immunity, but studies in vivo are not conclusive. Here, we investigated degree of polymerization (DP) dependent effects of β2→1-fructans on immunity via microbiota-dependent and -independent effects. To this end, conventional or germ-free mice received short- or long-chain β2→1-fructan for 5 days. Immune cell populations in the spleen, mesenteric lymph nodes (MLNs), and Peyer's patches (PPs) were analyzed with flow cytometry, genome-wide gene expression in the ileum was measured with microarray, and gut microbiota composition was analyzed with 16S rRNA sequencing of fecal samples. We found that β2→1-fructans modulated immunity by both microbiota and microbiota-independent effects. Moreover, effects were dependent on the chain-length of the β2→1-fructans type polymer. Both short- and long-chain β2→1-fructans enhanced T-helper 1 cells in PPs, whereas only short-chain β2→1-fructans increased regulatory T cells and CD11b - CD103 - dendritic cells (DCs) in the MLN. A common feature after short- and long-chain β2→1-fructan treatment was enhanced 2-alpha-l-fucosyltransferase 2 expression and other IL-22-dependent genes in the ileum of conventional mice. These effects were not associated with shifts in gut microbiota composition, or altered production of short-chain fatty acids. Both short- and long-chain β2→1-fructans also induced immune effects in germ-free animals, demonstrating direct effect independent from the gut microbiota. Also, these effects were dependent on the chain-length of the β2→1-fructans. Short-chain β2→1-fructan induced lower CD80 expression by CD11b - CD103 - DCs in PPs, whereas long-chain β2→1-fructan specifically modulated B cell responses in germ-free mice. In conclusion, support of immunity is determined by the chemical structure of β2→1-fructans and is partially microbiota independent.

Keywords: germ-free mice gut microbiota mucosal immunology prebiotics β2→1-fructans.


How to Intermittent Fast Safely

To follow the 16:8 intermittent fasting plan safely, you need to make sure to stay well hydrated while not eating by drinking plenty of water. Coffee or unsweetened green tea may be consumed in the morning to help fuel your workout (or you can use Pre-Workout), as long as you are not adding any cream or sweeteners.

There is some thought that consuming aBCAA supplement right before your fasted workout can help to prevent muscle loss. 1

When you’re in the 8-hour eating period, it’s crucial to obtain high quality meals containing all of your necessary macros (protein, carbs and fat) and vitamins/minerals for the day. Be sure to stay hydrated and meet your protein needs to prevent any lean muscle loss. It may be more difficult to obtain adequate calories in a short period of time, which may lead to weakness or dizziness. 3

Additionally, be cautious of not overeating just because you know you have another 16-hour fasting period ahead. Intermittent fasting is designed to keep your body in deficit for the day as a whole, so be cautious not to binge on high-calorie junk foods. 6

While there are promising outcomes of intermittent fasting, there’s an opportunity for further research related to performance and health benefits. 3 Many of the studies thus far were on overweight- or all-male subjects.

If you have blood sugar control issues, like diabetes or hypoglycemia, intermittent fasting may not be a good fit. Alternatively, if you are pregnant or breastfeeding, or take medications that are taken with food, speak to you doctor before trying the 16:8 diet.


Research reveals not all fasting diets are created equal

Three new studies published recently in the journal Cell have investigated the effects of fasting on different immune system mechanisms. The research reveals significantly different immune responses can be generated depending on the type of fasting studied, suggesting not all fasting diets are created equal.

It’s reasonable to be a little confused over the variety of fashionable fasting diets these days. From extreme multi-day, water-only fasts, to time-restricted intermittent feeding strategies such as only eating across a six-hour period every day, it is clear these diets have notable metabolic effects on the human body. But it is only recently that scientists have begun to explore the differences between these fasting cycles, and in particular the effect of these dietary strategies on the immune system.

Across three newly published studies, scientists have shown how certain fasting models can result in potent changes to immune system mechanisms. However, each diet can result in differing, and even opposite, immune effects, suggesting fasting diets need more accurate definitions in future research.

One study examined the effects of calorie restriction on the activity of memory T cells in mice. The research discovered enhanced T cell protection against infections and tumors when an animal’s caloric intake was reduced by 50 percent.

Another study looked at the effect of complete short-term fasting on monocytes, a pro-inflammatory immune cell, in both human and mouse models. The study found a short-stretch of fasting in both humans and mouse models resulted in less circulating monocytes and lowered monocyte inflammatory activity.

This, of course, is a useful observation if applied to someone suffering from a chronic inflammatory condition, but how does this immune system impairment affect a healthy body’s ability to heal wounds or fight off an infection?

The second study examined this question by comparing the immune effect of short-term fasting to longer term starvation on a mouse’s ability to fight off infection. While short-term fasting (less than 24 hours) did not compromise an animal’s ability to heal a wound or fight off infection, longer fasts did indeed begin to cause problems. When starved for 48 hours before skin injury or infection, significant immune response impairments were noticed.

The final study also investigated the effect of complete fasting on immune response in mouse models. This third study focused on gut immune response after fasting in young, healthy mice. Here the researchers were interested in understanding whether repeated stretches of fasting had detrimental effects on gut immune response in otherwise healthy animals.

Juvenile mice displayed significant immune system impairments after repeated 36-hour fasting stretches. In these young mice fasting seemed to have a detrimental effect on their immune system, exacerbating metabolic dysfunction and promoting allergic responses.

“… we found that food intake secures the integrity and function of the gut mucosal immune system through nutritional signaling,” write the researchers in the conclusion to their study. “Nutritional deprivation impairs mucosal immunity, leading to immune barrier dysfunction and excessive allergic response.”

What all this research means is that fasting diets may not be beneficial for everyone, and different kinds of fasting can result in drastically different kinds of immune system responses. In an editorial response to these three studies, researchers Roberta Buono and Valter Longo suggest the differing results demand more precise future research and clarity over different fasting strategy definitions.

“…the three new studies demonstrate the ability of different forms of fasting, as well as different lengths of fasting, to cause potent but distinct and at times opposite effects on the levels and function of various immune cell types, thus underlining the need to replace terms like fasting, or intermittent fasting, with those that describe the type and length of the fasting method such as a 24 h alternate-day fasting (12 H ADF), a 12 h time-restricted feeding (12 H TRF), or a 5-day fasting- mimicking diet (5-day FMD),” write Buono and Longo.


Pretreatment with rituximab does not inhibit the human immune response against the immunogenic protein LMB-1

Purpose: Rituximab, a humanized monoclonal antibody directed to the CD20 antigen present on B lymphocytes, could potentially abrogate the humoral immune response to murine monoclonal antibodies or immunotoxins by depleting antibody-producing B cells.

Experimental design: A Phase II study of LMB-1, an immunotoxin targeting the Lewis Y tumor antigen, in combination with rituximab was conducted to test the hypothesis that rituximab could abolish or diminish the development of human antibodies to LMB-1. Five patients were treated in this study and received 375 mg/m(2) rituximab on days 1 and 7 followed by 45 micro g/kg/day LMB-1 on days 10, 12, and 14. The development of human antibodies against LMB-1 was detected using a serum neutralization and ELISA.

Results: All five of the patients had a total suppression of circulating CD20/CD19 B-cell population before the administration of the first dose of the immunotoxin. Before rituximab treatment, the mean percentage of CD20/CD19-positive B cells in the five treated patients was 19.8% (range, 4.5-29.8%) of the total peripheral lymphocytes. After two doses of rituximab, CD20/CD19-positive B lymphocytes constituted </=0.1% of the total peripheral lymphocytes. Despite absent circulating antibody-producing B cells, before and during LMB-1 treatment, all of the patients developed neutralizing antibodies to the immunotoxin by day 21 of drug administration, which prevented retreatment.

Conclusions: Even though rituximab caused complete depletion of circulating CD20/CD19-positive B cells, it had no effect in suppressing the human antibody response to LMB-1 and may be of limited utility in suppressing human antibody responses to other immunogenic proteins.


An immune response is generally divided into innate and adaptive immunity. Innate immunity occurs immediately, when circulating innate cells recognize a problem. Adaptive immunity occurs later, as it relies on the coordination and expansion of specific adaptive immune cells. Immune memory follows the adaptive response, when mature adaptive cells, highly specific to the original pathogen, are retained for later use.

Granulocytes include basophils, eosinophils, and neutrophils. Basophils and eosinophils are important for host defense against parasites. They also are involved in allergic reactions. Neutrophils, the most numerous innate immune cell, patrol for problems by circulating in the bloodstream. They can phagocytose, or ingest, bacteria, degrading them inside special compartments called vesicles.


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Watch the video: Immune System (February 2023).