Cell Epitopes and Cell Proliferation
Independent B Cell Responses
The spleen cells are then removed and combined with a myeloma cell line using polyethylene glycol (PEG). Those spleen cells that do not fuse with the myeloma cell die within a day of being cultured. Then the confluent cells are subjected to selection using HAT (hypoxanthine, aminopterin, thymidine) medium.
Aminopterin blocks specific metabolic processes, but with the help of the intermediate metabolites (hypoxanthine and thymidine), spleen cells are able to complete these processes using auxiliary pathways. In this way, only the successfully fused cells will be able to survive several days of culture on HAT medium. If the result is positive, the hybridoma cells are subcloned several times to ensure clonality; where the specificity of the produced antibody is checked after each round for subcloning.
Such B-cell responses are usually of the IgM type, since switching to different classes of isotypes is either impossible or very inefficient in the absence of T-cell help.
Cell Activation
These paracrystalline patterned antigens are able to induce B-cell responses without contact-dependent T-cell help. The IgM response is of relatively short duration (showing a half-life of approximately 24 hours), but can nevertheless be highly effective. Important costimulatory signals are provided by binding of B7 (B7.1 and B7.2) proteins (present on the APC or B cell) to ligands on the T cells (CD28 protein, CTLA-4) or by CD40-CD40 ligand interactions.
Cell Activation by Superantigens
Stimulation of the T cell via the T cell receptor (TCR; Signal 1) activates a tyrosine kinase, which in turn activates phospholipase C (PLC). It also allows the induction of a process of somatic mutation and probably increases the survival of the B cell in the form of a memory B cell. Perforin-dependent cytolysis is important for the control of non-cytopathic viruses, tumors and transformed cells, but also plays a major role in the control of highly virulent viruses that produce syncytia (eg, smallpox virus).
IL-9 IL-9R,cc T cells Effect on mast cells. especially murine TH2), macrophages, Epstein-Barr virus. These contribute to the recruitment of "inflammatory cells" (eg, monocytes) to inflamed tissues and influence the recycling of all classes of leukocytes (Table 2.6). Lymphocytes can nonspecifically bind IgG antibodies via Fc receptors, then specifically attack target cells (eg, infected or transformed cells) using the bound antibody.
The objectives of the immune response include: inactivation (neutralization) and removal of foreign substances, microorganisms and viruses; rejection of exogenous cells; and preventing the proliferation of pathologically altered cells (tumors).
Cell Tolerance
Most self-antigens not present in serum or in lymphohematopoietic cells belong to this category and are ignored despite being potentially immunogenic. It has also been postulated that the naïve T and B cells that encounter antigens in the periphery will be anergized or inactivated due to a lack of the so-called costimulatory or secondary signals at these sites. For example, a relatively short period of immunosuppression after transplantation may allow the establishment of numerous dendritic cells from the transplanted organ in the recipient's secondary lymphoid organs, resulting in the subsequent elimination of the recipient T cells that react against foreign MHC molecules.
Many self-antigens are ignored by CD8+ cells. A transgenic mouse encoding a viral glycoprotein gene. For comparison with the many self-antigens present in peripheral non-lymphoid organs and cells, a gene encoding a viral glycoprotein (GP) was incorporated into mice, under the control of a regulatory gene that restricts GP expression only within the insulin-producing cells of the pancreas. When the GP expressing transgenic mouse was infected with a virus encoding the GP gene, which infects lymphoid organs, GP-specific cytotoxic T cells were induced and these cells destroyed the transgenic islet cells, resulting in the emergence of diabetes. This model showed that many self-antigens are ignored by the immune system simply because they are only present outside the lymphatic system.
In summary, T cell unresponsiveness can be achieved by: negative selection in the thymus; by excessive induction in the periphery; or by storage of the antigen outside the lymphoid organs.
Cell Tolerance
It is not yet clear whether the difference between a primary and secondary immune response is solely the result of the increased number of antigen-specific B and T cells and their acquisition of "memory properties", or whether immune protection is simply due to ongoing antigen-induced activation (Table 2.8). There is no surface marker that can unequivocally distinguish between memory T and B cells and "naïve" (never previously activated) cells. Instead, immunological memory is normally taken to correlate with an increased number of specific precursor T and B cells.
Even so, the precursor cells can only be activated (or reactivated) by antigen, and only activated T cells can provide immediate protection against re-infection outside the lymphatic organs, e.g. in the solid peripheral organs. As a general rule, the level of protective immunity mediated by the existence of memory T and B cells per se is minimal. Thus, secondarily activated (protective) memory T and B cells cannot be easily distinguished from primarily activated T and B cells.
Indeed, the antigen-dependent nature of immunological protection calls into question the relevance of a specialized “memory quality” of B and T cells.
Cell Memory
Cell Memory
Newborn mice require approximately three to four weeks (humans three to nine months) before the T-cell immune response and the process of T-B cell cooperation that leads to the generation of antibody responses become fully functional. Instead, an accumulation of the immunological protective antibodies that represent the immunological life experience of infections in the mother's serum is necessary. Memory T cells are nevertheless important in the control of intracellular bacterial infections (eg, tuberculosis [TB], leprosy), as well as persistent noncytopathic viruses such as hepatitis B and HIV (see also p. 106).
Paradoxically, the process of immunological cell destruction would allow the virus to survive for a longer period of time in the host and thus facilitate its transmission. The immune system, in a manner similar to that of many strictly extralymphatic self-antigens, initially ignores such tumors. amplifier;. Immune defense against infection and tumor immunity 107. amp; Congenital or acquired immunodeficiency – whether caused by antilymphocytic sera, cytostatic drugs, gamma radiation, UV radiation or infection – usually stimulates tumor growth, especially in lymphohematopoietic tumors.
Interestingly, experimental carcinogens are often also immunosuppressive. amp; Surgical removal of a large primary tumor may result in eradication. or rarely rapidly growing) of metastases within the lymph nodes.
IgE-Triggered Anaphylaxis
For example, chronic parasitic infections or malaria infections can lead to the development of Burkitt's lymphoma, a malignant B-cell disease. These mediators can affect smooth muscle and cause mainly pulmonary and broncho-postcapillary venule constriction, along with arteriolar dilation. Local signs of IgE-triggered anaphylaxis include burning of the skin (urticaria), diarrhea in food allergies, rhinitis or asthma in pollen allergies, or generalized anaphylactic shock.
Common causative agents of IgE allergies in humans include pollen, animal dander, house dust (mites), insect bites and stings, penicillin and food. Atopy correlates with high levels of IgE production, and desensitization refers to attempts to change a TH2 (IgE-producing) response into a TH1 (IgG-favoring) response through repeated vaccinations or oral doses of allergens (see Fig. 2.14, p. 78). It is likely that increased production of IgG - as opposed to IgE - antibodies plays a major role in the success of desensitization.
Little research has been done on the nature of the protective function of IgE during parasitic infections (or on the role of eosinophils).
Cytotoxic Humoral Immune Responses
Anti-hormone – Anti-thyroid hormone (Hashimoto thyroiditis) – Anti-intrinsic factor (pernicious anemia) Anti-drug – Chemical groups (haptens) bound to the cell surface. cytolysis, agranulocytosis) Anti-cell component – Anti-DNA (lupus erythematosus, LE). Therefore, intensive research is currently focused on the mechanisms by which T cell help to autoreactive B cells is regulated; Table 2.12 summarizes some of the possible mechanisms. These so-called "natural" antibodies (meaning that these antibodies are produced without a recognizable immunization process) are of the IgM class.
The presence of blood group antibodies makes blood transfusions between mismatched individuals extremely risky, making it necessary for the blood group of both donor and recipient to be determined before the blood transfusion takes place. During birth, small amounts of the baby's blood often enter the mother's bloodstream. Should the child's blood cells have paternal antigens that are missing from the mother's blood, his or her blood will effectively 'immunize' the mother.
If the danger of rhesus immunization is recognized at the end of the first pregnancy, the immunization of the mother can be prevented by passive infusion of antibodies against the child's antigen immediately after birth.
Diseases Caused by Immune Complexes
Where they meet, precipitation lines (known as precipitin bands) develop, indicating immune complex formation.a The antibodies precipitate identical epitopes (epitope 1) of both antigens, leading to the formation of precipitin bands that converge to form an arch, mutually migrating inhibit. The IgE concentration in the patient serum is then calculated based on a standard curve previously established by progressively “diluting” the IgE* test solution with unlabeled IgE. In this way, the percentages of the subpopulations in the total population can be determined.
LPS: lipopolysaccharide; a component of the cell wall of certain Gram-negative bacteria that acts as a B-cell mitogen. As a free substance, or bound in the LPS complex, it stimulates – by binding together with the LPS-binding protein (LBP) to the CD14 receptor of macrophages – the formation and secretion of cytokines that determine clinical endotoxin symptomatology. They are anchored in the outer membrane of the cell wall and extend radially from the surface.
Binds to uroepithelial receptors and to the P blood group antigen (hence "P" pili). In this phase, the bacteria's metabolism adapts to the conditions of the nutrient medium. The colony count method. The number of living cells in a given culture or material can be determined using the colony count method.
Cell-mediated Immunopathology
