Pathophysiology

• inflammation is relatively rapid, nonspecific, and short-lived.
• adaptive immunity is slower acting, specific, and very long-lived - it has memory.

immunoglobulins (antibodies) and lymphocytes (T and B cell)

Generation of clonal diversity

Clonal selection

The part of the immune response where B-cells produce antibodies in response to the antigens by way of activation of complement and phagocytes.

The process by which T cells undergo differentiation to develop effector cells that react directly with antigen on the surface of infectious agents. These effector cells include T-reg cells, Tc cells (cytotoxic), and memory cells.

• Produced by an individual after either natural exposure to an antigen or after immunization.
• Long lived
• Example is tetanus vaccine, or influenza vaccine.

• does NOT involve the host's immune response at all. rather it occurs when preformed antibodies or T lymphocytes are tranferred from a donor tothe recipient.
• short-lived or temporary because donors antibodies are eventually destroyed.
• Example: fetal-maternal placental transmission of antibodies.

Antigen

An antigen that induces an immune response resulting in the production of antibodies or functional T cells.

Epitope

• 1) foriegnness to the host (type of antigen)
• 2) size
• 3) adequate chemical complexity
• 4) present i nsufficient quantity

The large molecules of proteins, polysaccharides and nucleic acids or amino acids are more immunogenic.

Haptens

• 1) Circulating antibodies
• 2) BCR or B-cell receptor: antigen receptors on the surface of B lymphocytes.
• 2) TCR or T-cell recoptor: antigen receptors on the surface of T lymphocytes.

IgG

IgM

IgA: IgA1 is in blood, IgA2 is in body secretions

IgD

IgE

Complementary-determining regions (CDRs)

MHCs molecules are glycoproteins found the on the surface of all human cells except RBCs. They serve as the primary antigen presentation units of a cells.

Endogenous antigens derived from itracellular proteins by reacting with CD8 receptors on Tc cells.

Exogenous antigens derived from intracellular proteins by reacting with CD4 receptors on Th cells.

MHC class I, MHC class II, & CD1.

Exogenous lipid antigens derived from extracellular organisms.

Primary (central) lymphoid organs like the thymus and bone marrow.

The deletion of autoreactive T cells in the thymus.

• 1) B cells: present antigen to Th cells that facilitate development of the humoral immune response.
• 2) Macrophages: present antigen to memory Th cells in order to initiate a rapid response to antigens.
• 3) Dendritic cells: most effective in presenting antigen to naive immunocompetent Th cells. Immature dendritic cells function as phagocytes and carry processed antigen from the site of inflammation to the T-cell-rich areas of lymph nodes.

• 1) the antigen is of the appropriate type
• 2) the lymphocytes are prepared to recognize the presented antigen,
• 3) the antigen is presented appropriately

Helps the antigen-driven maturation of both B and T cells by facilitation and magnifying the interaction between APCs and immunocompetent lymphocytes.

• 1) Th cell directly interacts with the APC thru a variety of antigen-specific and antigen-independent receptors (TCR-CD4 receptors)
• 2) Th cell undergoes a differentiation process during which a variety of cytokine genes (IL-1) are activated
• 3) depending on the pattern of cytokines expressed, the mature Th cell interacts with either immunocompetent B or T cells to enhance their response to antigen. This results in differentiation into eithe rplasma cells or effector T cells, such as Tc cells.

Activate macrophages and Tc cells that leads to cellular immunity

Activate B cells that leads to the development of antibodies and humoral immunity.

Attraction on neutrophillsn and macrophages and induce chemokine protein production that leads to the inflammatory response.

Suppress the immune response by producing immunosuppressive cytokines to prevent the immune response from being excessive.

B-cell differentiation and proliferation. IgM antibody is the first to be detected in the circulation followed by IgG. The phase allows for clonal selection, antigen processing and presentation, induction of Th cells, interaction between immunocompetent B cells and Th cells, and the maturation and proliferation of the B cells into plasma cells and memory cells.

A more rapid production of a larger amount of antibody than the primary response due to the presence of memory cells. IgM is produced just as in the primary response. IgG, however, is produced in larger amounts compared to the primary response. Thus, IgG is the predominant antibody of the secondary immune response.

antibody-producing plasma ceslls and long-lived memory cells.

• 1) direct killing of foreign and/or abnormal cells (Tc cells)
• 2) assistance and/or activation of other cells, such as macrophages (T-reg cells and memory T cells)

• 1) Neutralization: inactivating or blocking the binding of an antigen to a receptor (neutralize bacterial toxins and viral toxins and opsonization of bacteria))
• 2) Agglutination: clumping of insoluble particles that are in suspension
• 3) Precipitation: making a soluble antigen into an insoluble precipitate

Enhance and activate several components of innate immunity (complement and phagocytes)

The process by which antibodies that make the pathogen more susceptible to phagocytosis thru binding to various receptors (Fc or C3b) on the phagocytes surface.

Tc cells or CTLs.

Tc cells kill malignant cells expressing MHC class I, NK cells kill abnormal cells with suppressed MHC class I expression.

Primary response is stronger because the immunoglobulin produced in utero is mostly IgM. The fetus is unable to produce IgG.

At age 5-6 months of age because the mothers antibodies from in utero are catabolized quicker than the infant can produce more. This is the age when infants are most at risk for infections.

• 1) Decreased T-cell activity
• 2) decreased mature T cells because the thymus is less able to mediate T cell differentiation (shift in populations of T cell subtypes)
• 3) decrease in B cell antibody production (less memory cells)
• 4) decrease in memory B-cells. (poorer long-term immunity)

• 1) Allergy: exaggerated against environmental antigens
• 2) Autoimmunity: misdirected agains the host's own cells
• 3) Alloimmunity: directed agains beneficial foreigh tissues, such as transfusions or transplants.
• 4) Immune deficiency: insufficient to protect the host.

Immediate hypersensitivity reactions

Delayed hypersensitivity reactions.

Anaphylaxis

• Mediated by IgE
• Products of tissue mast cells
• Allergy reactions - most occur against environmental antigens
• Most potent mediator is histamine

• contracts bronchial smooth muscles causing bronchial constriction
• increases vascular permeability causing edema
• causes vasodilation increasing blood flow into the affected area

• increased gastric acid secretion
• decrease of histamine released from mast cells and basophils

• 1) compliment mediated lysis with IgG or IgM antibodies
• 2) Opsonization/phagocytosis of the target cell caused by IgG and C3b opsonins that bind to receptors on the macrophage.
• 3) Neutrophil-mediated tissue damage due to antibody and complement attraction of neutrophils
• 4) Antibody-dependent cell-mediated cytotoxicity (ADCC) by NK cells that release toxic substances that destroy the target cell.
• 5) Modulation of cellular function causing the target cell to malfunction by reactions to the antibody binding alone.

• **Can be systemic or localized
• **Caused by antigen-antibody (immune) complexes that are formed in the circulation and deposited later in vessel walls or extravascular tissues.
• **Antibody binds to soluble antigen that was released into the blood or body fluids and then the complex is deposited into the tissues.
• **NOT organ specific
• **Attraction of neutrophils and subsequent release of lysosomal enzymes cause most of the resulting tissue damage.

The systemic prototype of Type III: immune complex-mediated hypersensitivity reaction.

Caused by the formation of immune complexes in the blood and their subsequent generalized deposition in target tissues.

Example is Raynaud phenomenon: caused by the temperature-dependent deposition of immune complexes in the capillary beds of the peripheral circulation.

The prototypic example of a localized immune complex-mediated inflammatory response.

Mediated by T lymphocytes and DO NOT involve antibodies.

Occur thru Tc cells or Th1 (lymphokine-producing) cells. Tc cells attack and destroy cellular targets directly. Th1 cells produce cytokines that recurit and activate phagocytic cells (macrophages).

Example: graft rejection and allergic reactions resulting from contact with poison ivy (contact dermatitis) and metals (atopic dermatitis)

It binds to specific receptors on smooth muscle and reverse the effects of histamine and result in muscle relaxation.

type O blood lacks both A and B antigens so anyone can accept their red blood cells.

Type AB blood lacks both anti-A and anti-B antibodies and can be transfused with any ABO blood type.

• CD4-positive Th cells
• dendritic cells
• macrophages
• CD8-positive Tc cells
• thymic cells
• NK cells

gp120 glycoprotein

It makes its way into the cytoplams of the infected cell and uses reverse transpriptase to convert its RNA to DNA.

the infected cell's nucleus

It is a viral enzyme that helps the virus (HIV) to integrate itself into the host cell's genetic material.