ACQUIRED++IMMUNITY

ACQUIRED IMMUNITY P. 796 onward in Marieb 6th Ed.

Characteristics:

Highly specific - has memory programmed for specific antigens Systemic

.............................Cell Mediated immunity
 * Two Components**: Humoral immunity = antibodies involved = antibody mediated

__**INFECTIVE AGENTS: ANTIGENS**__ Anything the body regards as strange/foreign : not from the self.

COMPLETE ANTIGENS: Immunogenicity = can generate an immune response on its own Reactivity = can react with activated lymphocytes & antibodies

INCOMPLETE ANTIGENS = HAPTENS = are too ‘small’ to have an effect when these chemicals link with body proteins they can mount an attack Thus: NO Immunogenicity but has reactivity. eg. many allergens - poison ivy, cosmetics, detergents, etc.

ANTIGENIC DETERMINANTS :

surface of antigen carries ‘specific markers’ for that particular antigen. The markers are ‘filed’ with certain lymphocytes to recognize them when they enter again

SELF-ANTIGENS: MAJOR HISTOCOMPATIBLITY COMPLEX (MHC) PROTEIN Markers on cells which are similar throughout the body of an individual but will differ from that of another individual. The body’s immuno-active agents recognizes its own MHC’s and will not attack it. Sometimes, with auto-immune diseases, the body’s cells ‘turns on itself’. Most cells of the body contain Class I MHC’s

Cells of the immune system contain Class II MHC’s NB These markers are not the ‘antennae’ that search for substances in the

environment to react to. The markers are like the ID-documents of the cell.

__ CELLS OF THE ADAPTIVE IMMUNE SYSTEM __

Lymphocytes Produced in bone marrow -

Those that migrate to the THYMUS to mature = T-cells

T-cells -play role in cell mediated responses

Thymic hormones ‘initiate’ lymphocytes into the immune responses. Those who quickly record the ‘antigen’ survive. Others will die off as they appear not to have a purpose. This can be seen as primary education of the T-cells and the ‘educated’ T - cells divide rapidly to produce a colony of the same type of cell [that recognizes a specific antigen] after a process of selection and deselection, T-cells that make it through these processes are deemed immuno-competent.

B-cells remain in bone marrow and migrate to spleen and lymph nodes or roam the blood system after becoming immuno-competent. Their activities involve production of antibodies amongst others. Both T & B immuno-competent cells migrate to lymph nodes, spleen and other lymphoid tissue as immature/naive lymphocytes. Upon contact with antigens they differentiate into antigen-activated lymphocytes.

Antigen-Presenting Cells (APC’s) Mostly dendritic cells present in conn. tiss. These include Langerhans cells in skin, macrophages and activated B-cells. Macrophages and dendritic cells secrete soluble proteins that activate T-cells. CAM’s - Cell Adhesion Molecules - helps with mobilization of specific lymphocytes to areas where they are needed.

__ THE HUMORAL IMMUNE RESPONSE __ antibody-mediated response Cloning of B-cells: Once activated by an antigen, a B-cell rapidly divides giving rise to an army (clone) of cells of the same type against a particular antigen. Most of these cells become plasma cells which are rather short-lived as they are formed to fight an antigen and work hard at that. Some of the clonal cells remain ‘dormant’ and live much longer. They function as memory cells that will be ready when they encounter another antigen of the same type in future.

Primary immune response - antibody formation - lag period (latent phase) of about 3 - 6 days during which activated B-cells proliferate with their antibodies. Reaches peak after about 10 days and then declines. Secondary immune response - memory cells of first attack are mobilized upon a next encounter. They already have the message and can copy it very quickly to form an army of plasma cells within 2 - 3days at levels much higher than primary response.
 * IMMUNOLOGICAL MEMORY**


 * Active Humoral immunity** is acquired upon contracting bacterial or viral infections naturally


 * Passive Humoral immunity** is acquired by artificial infections eg. Vaccinations. The problem with vaccination is that the route followed is a weaker route, targets different T-cells and the effects are vastly different from the response achieved through primary active infection - which produces much larger and much more vigorous clones and more memory cells. Education of the T-cells are hampered in this way. Thus the recurrent infections that may follow vaccinations. Vaccines makes use of dead or weakened pathogens - antigens may not be that threatening and the body’s response is mild. Vaccines may cause the disease it is trying to prevent, it may cause allergic reactions.


 * Antibodies** are on the surface of the B-cells, conforming to the shape of the binding site of the antigen. The antibody-antigen complex cannot bind to the cells and the antigen is thus inactivated, not destroyed. The macrophages and other phagocytes will have to destroy the antigens. Since the antibodies are structures in a particular way to fit the specific antigen, the antibody-antigen complexes may form aggregates/agglutinate and are less mobile, thus easier for attack by macrophages.

__ CELL MEDIATED IMMUNE RESPONSE __ diagram p 808 Marieb 6th Ed.

T-cells are the mediators and much more complex in organization - depending on the differentiation glycoproteins they can be **CD4 (T4) or CD8 (T8)** cells. In addition there are Ts - suppressor cells or **T-memory** cells and other less common ones. T-Cells operate on the basis of double recognition. It must recognise both MHC class I (the self) as well as the antigen (non-self ; doesn’t belong here) at the same time. T-cells are activated when its receptors (TCRs) binds to the antigen-MHC of the body cell.

CD4 (T-Helper cells) can only bind to antigens linked to Class II MHC proteins. Some APCs carry their antigens to the lymph nodes and other lymphoid tissue to present their antigens. In addition to this stimulation by the antigen - in whichever way it was presented, the T cell must receive a costimulus which can come from proteins on the macrophages. There are many ways of costimulation which must be effected before a T-cell will divide and build up an army/clone of cells against a specific antigen. If this fails, the T-cell becomes tolerant and allows the antigen to cause havoc if other T-cells do not stop it. The phagocytes will dispense with all debris of cells and antigens that become casualties of the fight against infection.


 * Cytotoxic T Cells = T killer cells**

These cells can directly attack and kill other cells. The roam the body in search of foreign bodies and attack these cells ‘on sight’.

They bind to the foreign cells and release perforin and granzymes into the membrane of the target cell.

Ca++ required to polymerize perforin molecules and create pores between T Killer cell and target cell.

Granzymes enter the target cell through the pores and break down cellular content resulting in cell death (apoptosis).

T-Killer cell then detaches and searches for other ‘prey’. T Suppressor cells release cytokinins that suppress the activity of the B-cells (antibody formation). These cells wind down and stop the immune response when necessary.

The use of these cytokinins is applied in suppressing organ rejection after transplant.

__**IMMUNODEFICIENCY**__ SCID = Severe Combined Immunodeficiency = congenital defect, drastic lack of T & B cells. AIDS = Acquired Immune Deficiency Syndrome Hodgkin’s disease =

Write a short description of each of these diseases.
 * AUTO-IMMUNE DISEASES (p. 819)**

Multiple Sclerosis- white matter is axon - myelin sheaths - degeneration causes defective nerve functioning --- loss of control of muscles



Brain and spinal cord .........................................................the affected affected here........................................................neuron

Person with MS - using alternative means of locomotion

Myasthenia gravis,



Graves Disease



Type I diabetes ;

Systemic Lupus erythematosus;..........................................................................................................................................Cutaneous/Subcutaneous Lupus



Glomerulonephritis ; Rheumatoid arthritis