Immunity

How immunity works???
Ans:Through antibodies, produced by B cells. Terminally differentiated B cells, called “plasma cells,” produce most of the antibodies. Humoral immune responses defend the host against extracellular bacteria and toxins. Blocking antibodies can prevent the adherence of bacteria, viruses, or toxins to host cells. Antibodies can activate complement through the classical pathway and lyse cells. Complement activation also generates chemotactic fragments that activate mast cells and phagocytes and chemotactically attract phagocytic cells into sites of inflammation. NK cells can bind to antibody-coated targets and lyse them in antibody-mediated cytotoxicity. Antibodies can also opsonize; in other words, their binding facilitates uptake of the antigen by phagocytic cells.
Through the action of T cells. CD8þ cytolytic T cells can kill target cells directly. CD4þ helper cells can activate macrophages to become more effective at killing the organisms they ingest. This process is also considered to be cell-mediated immunity, although, again, a cell of the innate system carries out the ultimate effector function. Cells of the innate system are also needed to initiate humoral and cell-mediated responses. Dendritic cells and macrophages ingest organisms, digest them into peptides, and present them to T cells and B cells in a way that causes antigen-specific lymphocytes to proliferate and differentiate into effector cells.

What are the features of primary and secondary immune response?
Ans: A primary antibody response occurs after the first exposure to an antigen, whereas a secondary antibody response occurs with the second and subsequent exposures. A secondary response is faster and bigger and contains antibodies that bind with higher affinity to antigen and a greater diversity of T cells that react with the target antigens. In a secondary response, the antibody levels increase and new effector T cells enter the circulation within 1–2 days. In contrast, during a primary response, the emergence of these elements of an adaptive response can take a week or more. During a secondary response, the quantity of antibodies and the number of effector T cells is increased 10-fold or higher. The average affinity of the antigen-binding sites is also higher in a secondary response. Finally, during a secondary response, more of the antibodies belong to the IgG class, whereas in a primary response most of the antibodies are IgM. Major features of these A primary antibody response occurs after the first exposure to an antigen, whereas a secondary antibody response occurs with the second and subsequent exposures. A secondary response is faster and bigger and contains antibodies that bind with higher affinity to antigen and a greater diversity of T cells that react with the target antigens. In a secondary response, the antibody levels increase and new effector T cells enter the circulation within 1–2 days. In contrast, during a primary response, the emergence of these elements of an adaptive response can take a week or more. During a secondary response, the quantity of antibodies and the number of effector T cells is increased 10-fold or higher. The average affinity of the antigen-binding sites is also higher in a secondary response. Finally, during a secondary response, more of the antibodies belong to the IgG class, whereas in a primary response most of the antibodies are IgM. Major features of these

Describe functions of the complement system?
Ans:The complement system functions as the innate part of humoral immunity by promoting inflammatory reactions, and it facilitates the effector functions of antibodies, especially IgM and IgG antibodies. C3b, generated by the cleavage of C3, binds to the surface of antigens, including microbes, and facilitates their uptake by neutrophils and monocytes that express a C3b receptor. C5a and, to some extent, C3a are chemotactic for neutrophils and monocytes and serve to recruit leukocytes into sites of inflammation. C3a and C5a are also known as “anaphylatoxins” because of their ability to induce mast cell degranulation. The terminal complement components, C6, C7, C8, and C9, form the membrane attack complex, a tubular structure that inserts through the plasma membrane of cells and microbes and kills them. Figure 11-4 summarizes specific functions of the complement system.