Immune System Review

I. Immune Cells – White blood cells

A. Phagocytes

1. Monocytes/Macrophages

- Monocytes – circulate, can be transformed into macrophages

- Specialized: microglial cells of brain, alveolar macrophages etc.

B. Granulocytes

1. Contain granules (cytotoxic substances)

2. Short lived - ~3 days

3. Neurophils (polymorphonuclear leucocytes)

- ~90% of the granulocyte population

- Phagocytotic like macrophages

4. Eosinophils

- Combat larger invading cells, attracted by IgE

5. Basophils

- Granules contain histamine

6. Mast cells

- Granules contain histamine

- Not generally found in circulation (found in spleen, skin, etc.)

C. T lymphocytes

1. Mature in the thymus

2. Cell-mediated immunity

3. T-helper and T-suppressor cells mediate Bcell response

4. Cytotoxic or “killer-T” cells

D. B-cells

1. Secrete antibodies – humoral immunity

2. Memory cells vs. plasma cell (secretes the antibodies)

II. Antibodies

A. Types of immunoglobins

1. IgG – main form of circulating antibodies

2. IgA – main form of antibodies found in milk, saliva

3. IgE – form of antibody responsible for allergic symptoms, hypersensitivity

4. IgM, IgD – antigen receptors on cell surface

B. Structure

1. “Y” shape

2. Two heavy chains, two light chains

3. Fc region (stalk) is not very variable

4. Fab region is the antigen binding region and is variable (provides specificity)

IIIa. Cortisol – endocrine review

A. Released from adrenal cortex (outer part of adrenal glands)

1. Hypothalamic-Anterior Pituitary-Adrenal axis

2. Hypothalamus responds to stress by releasing CRH (corticoid releasing hormone)

3. Anterior pituitary releases ACTH (adrenocorticotrophic hormone)

4. Cortisol exerts negative feedback on hypothalamus and ant pituitary

B. One of the glucocorticoids

1. Release stimulated by long term fasting, exercise, injury, stress

2. Promote breakdown of fats, gluconeogenesis, protein breakdown

3. Decrease non-CNS glucose uptake

4. Anti-inflammatant and immune suppressing

IIIb. Effect of Cortisol on Immune Function

A. Inhibition of phospholipase A2 (all glucocorticoids)

1. Via lipocortin

2. Phospholipase A2 is the enzyme that produces free arachidonic acid, the precursor to all prostaglandins, thromboxanes, and leukotrienes

B. Glucocorticoid inhibition of cell function and proliferation

1. Inhibit release of proteolyic enzymes from lysosomes (reduces swelling)

2. Inhibit differentiation and proliferation of mast cells

3. Cortisol decreases the phagocytic and bacteriocidal activity of neutrophils

4. Cortisol increases the release of neutrophils from the bone marrow

5. Cortisol decreases the number of circulating eosinophils

6. Cortisol decreases the proliferation of fibroblasts and the deposition of fibrils – prevents walling off of infection

7. Cortisol decreases the number of circulating Tcells, especially helper T’s

8. Overall, cell-mediated immunity is inhibited by cortisol

9. Cortisol inhibits the differentiation of monocytes into macrophages and secretion of IL-1 by macrophages

10. Cortisol suppresses fever prob via decreased production of IL-1

11. Cortisol does NOT appear to directly affect Bcell proliferation and differentiation or production f antibodies

12. Does not inhibit release of histamine by mast cells

IL-1 and other lymphocyte products stimulate ACTH secretion

Glucocorticoids are used for immune suppression, as in organ transplantation, autoimmune disease