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1 number Immunology Done by Tamara and Hiba Corrected by Rana Ghassan Doctor Sameer

2 Immunology In the development of cells, we have certain stages that take place: 1) Multi potential 1 hematopoietic stem cells will differentiate into a common myeloid progenitor, or a common lymphoid progenitor. Lymphoid progenitors are responsible for the formation of lymphocytes, while myeloid progenitors are responsible for the formation of white blood cells, red blood cells and platelets. 2) Common lymphoid progenitors can then differentiate into small lymphocytes or natural killer cells which are very important in eradicating viral infections. The small lymphocytes can then further differentiate into B-lymphocytes and T- lymphocytes. B-lymphocytes can also undergo further differentiation to produce plasma cells which give rise to the antibodies. 3) Myeloid progenitors on the other hand can differentiate into megakaryocytes which produce thrombocytes (platelets) for blood clotting, erythrocytes (red blood cells), mast cells, and myeloblasts which give rise to basophils, neutrophils, eosinophils, and monocytes that form macrophages. The figure below further clarifies the previous points: 1 Multipotential cells: cells that are essentially committed to produce specific cell types and have a limited ability to differentiate such as those of the brain.

3 Phases of an Immune Response: In general, the immune responses in our body either involve B-cells, or T-cells. Both B-cells and T-cells start as naïve B and T cells; meaning cells that have never encountered an infection before. When an infection develops, they will be activated by microbes. The naïve T-cells can then form effector T-cells which function during the infection. At the end of the infection, the effector T-cells will develop into memory T-cells which are responsible for long-lived protection. On the other hand, the naïve B-cells will form plasma cells that are responsible for rapid protection during the infection secreting high amount of antibodies (immunoglobulins). At the end of the infection, plasma cells will differentiate into memory B-cells which are responsible for the long-lived protection against microbes. This concept is mostly related to vaccines, where some vaccines like the ones against tuberculosis mainly target T-cells, while other antiviral and antibacterial vaccines mainly target the B-cells and the secretion of immunoglobulins. It is important to note that in our body, both the T-cells and B-cells cooperate and one system can interact with and activate the other. Immunity to microbes: The host defense mechanisms against microbes could either be specific, or non-specific (innate immunity). our defense system starts with non-specific immunity also called

4 innate immunity which is composed of the everyday mechanisms that help protecting us against invaders, where they are always working in the background no matter what pathogen we are exposed to which is where the name non-specific came from. Examples include the skin, cilia in the airways, hairs in the nose, tears and etc. Specific immunity also called adaptive immunity is the specialized form of immunity against pathogens which includes the T-cells and B-cells. It is called adaptive because you (don t born with it ) like innate immunity; you have to be exposed to pathogens first to acquire this type of immunity. This means that innate immune response controls infection long enough for adaptive responses to kick in, and can often eradicate the infection. If the innate immune response fails to eradicate the pathogen, interleukins in this case will be produced which will stimulate the T-cells, thereby activating the adaptive immunity. In other words: Many pathogenic microbes resist innate immunity Adaptive immunity is able to combat these microbes -- the lymphocyte expansion that is characteristic of adaptive immunity helps to keep pace with rapidly dividing microbes; specialized immune responses are better able to deal with diverse microbes. So, theoretically speaking, all microbes that invade our body must be combated by our immune system. Effector mechanisms against microbes: The immune system is specialized to generate different effector mechanisms for different types of microbes: 1- Extracellular microbes 2- Intracellular microbes Intracellular microbes are mainly viruses, while bacteria and fungi are mainly extracellular microbes. We can easily combat extracellular microbes through phagocytosis and antibodies, while intracellular microbes can be attacked by cytotoxic T- lymphocytes, T-helper cells, and sometimes phagocytes.

5 Innate immunity mechanism: The body has defenses which are not specifically directed at particular infectious agents, but which serve as non-immunological barriers to infection: 1) Skin- an effective and impermeable barrier unless breached by injury, disease, etc 2) Respiratory tract- upwards flow of mucus by ciliated epithelium removes virus particles, to prevent invasion of the lower respiratory tract, where the microbe can be expelled through sputum. In infections mostly, we realize that the production of mucus increases. 3) Gastrointestinal tract- stomach acid inactivates acid-labile viruses, where the ph of the stomach is as low as 2. Bile (lyses enveloped viruses), movement of intestinal contents, and uptake of virus by lymphoid tissue all aid elimination of ingested viruses. E.g.: Lymphoid granules called peyer s patches(lymphoid follicles) are mostly found in intestines, which play an important immune role against poliomyelitis infection. 4) Urinary tract- flow of urine exerts a protective flushing effect. This is why people with urinary tract infections are advised to drink large amounts of water; to provide a mechanical pathway for flushing the microbes out of the body. 5) Conjunctiva- lacrimal glands produce tears which flush viruses from the eye and drag it down the nasal cavity. 6) Phagocytosis: an important defense mechanism in bacterial infection and in virus infections also: invading viruses- like bacteria- are ingested by two types of scavenger cells: a) Neutrophil polymorphonuclear leukocytes (PMN).

6 b) Macrophages (or mononuclear cells of the reticuloendothelial system) - of two types: Free macrophages in lung alveoli, peritoneum. Fixed macrophages in lymph nodes, spleen, liver (Kupffer cells), connective tissue (histiocytes) and CNS (microglia). Note: During inflammation, neutrophils are the first to be activated since they continuously circulate in the blood, while macrophages reside in tissues. Phagocytosis can be enhanced in two ways: 1. By antibody (a specific immune mechanism) and complement: this effect is known as opsonization. To clarify, immunoglobulins (antibodies) have two portions( mainly the Fc portion that can interact with macrophages and neutrophils) to drill holes in the cell membranes of microbes thereby killing them; this is opsonization. So, when we have another factor like opsonization interfering with the killing process, it will greatly enhance phagocytosis. 2. Macrophages activated by cytokines (interleukins) released by T lymphocytes - a specific immune mechanism- have increased phagocytic activity and are attracted by chemotaxis to the site of infection providing more rapid immunity. Cytokines:

7 Cytokines are small protein molecules released by many cells, including lymphocytes and macrophages: they function as signals or mediators to: a) activate b) modulate c) And control the immune responses (and other activities) of cells. There are numerous cytokines, e.g. interferons, interleukins and tumor necrosis factor(tnf): many act sequentially and interact with other cytokines. In addition to their role in the immune response, some have physiological functions such as tissue repair, differentiation and signaling activity in the CNS. Interferon as Body Defense Mechanism: These are small proteins produced by certain cells. They have 3 main types: a) Alpha interferon- produced by lymphocytes & macrophages b) Beta interferon produced by fibroblasts & epithelial cells c) Gamma interferon produced by T cells (specific immunity) You should know three important things about interferons: 1) They are produced in response to viruses, RNA, immune products, and various antigens 2) They bind to cell surfaces and induce expression of antiviral proteins 3) They Inhibit the expression of cancer genes Mechanism of action of Interferons: Induction of the following enzymes: 1) a protein kinase which inhibits protein synthesis 2) an oligo-adenylate synthase which leads to degradation of viral mrna 3) a phosphodiesterase which inhibit t-rna The action of these enzymes leads to an inhibition of translation The doctor said that this part is not important because we will be taking it later on in immunity, so just read it.

8 Specific Immunity: Immunological responses are of two types: 1) Humoral- main effect is neutralization of viruses: responsible for protective immunity. Neutralization refers to the antibody-antigen interaction that occurs. 2) Cellular- main effect is localization of lesions: kills virus-infected cells. When we say humoral we are talking about immunoglobulins while when we say cellular we are mainly talking about T-lymphocytes. Humoral (Antibody) Response: Like other infectious agents, viruses induce production of antibodies in the blood. Antibodies are: 1) Immunoglobulins: Proteins which react specifically with antigens; the same way a key can open only one lock, each antibody is specific to each antigen. They are also usually proteins and the most important ones in protective immunity are those on the surface of virus particles. 2) Plasma cells: formed when B-lymphocytes are activated by encounter with antigen. B- lymphocytes have immunoglobulins on their surface, which act as receptors for virus antigens. Helper T cells contribute to the differentiation of B- cells into plasma cells, so they help B-cells to produce immunoglobulins. Antibodies: 1. Immunoglobulin (Ig) 2. A large Y-shaped protein 3. Consists of 4 polypeptide chains

9 4. Contains 2 identical fragments (Fab) with ends that bind to specific antigen 5. Fc binds to self There are 5 main types of immunoglobulins generally, 4 of them are always circulating in the blood while 1 is found at a much lower concentration in the blood because it is surface bound, and this one is IgD. Three Immunoglobulins are mainly responsible for Humoral immunity in virus infections. 1) IgM- the earliest antibody produced: appears at a variable interval after exposure, depending on the virus, incubation period, dose and route of transmission; persists for about 4-6 weeks, sometimes longer; a pentamer of five IgG molecules. It is not a high affinity antibody. If you were asked about the first antibody to be produced, then it would be IgM. It is also the largest antibody so it doesn t cross the placental barrier so it doesn't transmitted from the mother to the fetus and vice versa. 2) IgG- formed later than IgM but persists long term, often for years: responsible for immunity to reinfection. Unlike IgM, IgG can cross the placental barrier. So, if you administer a vaccine for measles to a 70-year old and you find measles antibodies in his body after a while, you should know that these antibodies are IgG because they are long term. 3) IgA- A dimeric molecule, found in body secretions (as well as blood), i.e. saliva, respiratory secretions, tears and intestinal contents; the main antibody involved in immunity to respiratory viruses, GIT infections and uro-genital tract infections, and in gut immunity associated with enteric virus infection; secretory IgA acquires a carbohydrate transport piece in extracellular fluids that is absent from serum IgA.

10 Side note: We also have IgE, for allergic reactions. All allergy tests depend on the presence of IgE. Note: You can memorize them through the word MAGED or GAMED. Cell-mediated immunity: Cellular immunity plays an important part in the response of the body to viruses. Children with congenital deficiency of cellular immunity are abnormally susceptible to virus infections and often (although not always) develop unusually severe diseases: those with humoral immune deficiency, on the other hand, respond normally to virus infections. Why? Because viruses as we mentioned are attacked by T-cells while bacteria is attacked by antibodies (immunoglobulins). For example like HIV viruses. Cell-mediated immunity is the mechanism for the elimination of virus-infected cells- and therefore virus- from the body. T- or thymus-dependent lymphocytes are the principal cells involved in this. There are two main types: 1) CD4-positive helper T-cells 2) CD8- positive cytotoxic T-cells. Both CD4 and CD8 T-cells can cooperate and interact with one another. Antigen Processing and Presentation: In order for our body to be able to detect antigens, these antigens must be carried with another substance which is called MHC. It distinguishes between self and non-self, where the clinical importance of this applies to organ transplants when we want to test whether the donor organ matches the recipient or not. We carry out something called the HLA (human leukocyte antigen) typing for MHC to know whether the organ is self and therefore accepted by the recipient or non-self and therefore denied. MHC has three types, but we should only know that MHC I is found in all cells, while MHC II is found only in macrophages, dendritic cells, and in some T and B cells.

11 Cell-mediated immunity : (continued) 1) CD4-positive helper T-cells- carry CD4 receptors as markers on their surface. The most important cells in the cellular response, they liberate cytokines that activate and modulate cellular immune responses. They require MHC (Major Histocompatibility Complex) class II antigens to be presented in association with the target antigen for their activation. They also interact with B-lymphocytes for antibody production. 2) CD8-positive cytotoxic T-cells- carry the marker CD8 receptor on their surface and are MHC Class I antigen-restricted. They lyse target cells such as virus-infected cells and tumor cells; the main mechanism for elimination of virus-infected cells from the body; also release cytokines. Suppressor function: note that both CD4 and CD8 cells can suppress as well as activate the cellular response. The importance of this is to inhibit immune reactions when they are not needed to avoid damage of cells. After an antigen is removed, the T and B cells will acquire memory of that antigen so that antibodies are quickly produced against it the next time it infects the cell. A virus is recognized as an antigen by helper T-cells when presented by a macrophage or dendritic cell (found in lymph nodes and skin) acting as an antigen-presenting cell: recognition is dependent on MHC Class II antigens.

12 Properties and roles of memory cells: Survive even after infection is cleared Numbers are more than naïve cells Respond to antigen challenge (recall) more rapidly than do naïve cells Memory T cells: migrate to tissues, some live in mucosal tissues and skin Memory B cells: produce high affinity antibodies Provide rapid protection against recurrent or persistent infections Goal of vaccination is to induce effective memory Roles of antibodies and CTLs in adaptive immunity to viruses Antibodies neutralize viruses and prevent infection Block infectious virus early in course of infection (before entering cells) or after release from infected cells (prevent cell-to-cell spread). CTLs kill infected cells and eradicate reservoirs of established infection In some latent viral infections (EBV, CMV). Latent means that the virus is found in the dorsal root ganglia in the nervous system, and when the immune system is suppressed, it will be activated. CTLs control but do not eradicate the infection; as we said, defective T cell immunity leads to reactivation of the virus (in HIV, immunosuppression caused by leukemia, treatment for graft rejection). Immune evasion by viruses: Antigenic variation (also called shift and drift) Influenza, HIV, rhinovirus, for example the H1N1 virus undergoes antigenic variation every 10 years which means that vaccines cannot always guarantee a 100% protection. Inhibition of the class I MHC antigen processing pathway Different viruses use different mechanisms NK cells are the host adaptation for killing class I MHC-negative infected cells Production of immune modulators Soluble cytokine receptors may act as decoys and block actions of cytokines (poxviruses) Immunosuppressive cytokines, e.g. IL-10 (EBV) Infection of immune cells HIV

13 Efficacy of vaccines: Vaccines have been useful for generating protective antibodies, but so far, not for generating effective cell-mediated immunity. This means that vaccines can help us produce antibodies only. Vaccines work best against microbes that: 1. Do not vary their antigen 2. Do not have animal reservoirs. Why? Because animal reservoirs like influenza virus can easily have antigenic alterations. 3. Do not establish latent infection within host cells 4. Do not interfere with the host immune response

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