1. Multiple layers of protection
Ch 43 Our Immune system
Highly sophisticated
Multiple layers of protection
Millions of disease-specific cells that clone and defend us from sickness and death

2. We are born with certain protections and we acquire others during life
3 lines of defense against disease:
1. Innate protection: skin, mucus membranes
severe pH’s
enzymes
phagocytes

3. 2nd line: inflammation Skin breached Non-self cells targeted
Phagocytes
Non-specific
Histamines incr blood flow
Chemokines attract phagocytes

4. Interferons a, b are pt of innate defense
They’re juxtacrine chemical messengers, telling neighbors to produce defensive enzymes against pathogens.
Complement systems: serum proteins activated by non-self substances (lyse pathogens)

5. Non-specific Killer cells include macrophages, neutrophils, dendritic cells Natural Killer…
Always on patrol for non-self cells.
Pathogens’ ability to mask presence reduced by interferons.

6. The lymphatic system circulates many of the substances that fight infections

7. Acquired Immunity- defense against specific pathogens
Function of lymphocytes (B or T)
Recognize antigen molecules
“designer destroyers”, ie, they’re specific

8. WHAT IS AN ANTIGEN?
A substance that produces an immune response in an(other) organism
An antigen’s epitope

9. Lymphocytes are either B or T type.
Both have antigen receptors rooted to their cell membranes
B’s are ‘Y’-shaped, made of 4 polypeptide chains
Have Variable and Constant sections
Every B cells’ is different

10. The B lymphocyte antigen receptor

11. T lymphocyte antigen recept’s
Always attach to cells that they are defending against
2 straight PP chains (not 4), with variable tips
Can recognize antigen fragments on the Cl 1 MHC ( major histocompatability complex) molecule common on most cells

12. Kill cells infected w/pathogens, cancer cells, transplants...
Cytotoxic T cells (CD8’s) recognize antigens displayed by Class 1 MHC molecules.
Kill cells infected w/pathogens, cancer cells, transplants...
Major histocompatability complexes APC = antigen presenting cell CD 4. 8 are proteins

13. Class II MHC are found on phagocytes (antigen presenting cells)
MHC2 present antigen fragments to Helper T cells which connect using CH4 molecules, then communicate to B cells to produce antibodies.

14. MHC molecules’ importance
Genetics has most allelic diversity of all phenotypes. SO…
Everyone but identical twins has unique heterozygous genotype for MHC markers.
Everyone’s V & J segments can be rearranged

15. Humoral immune responses attack infections outside of infected host cells.
Helper T cells read MHC class 2 displays on APC’s with the CD4 protein.
Release cytokine messengers to B’s, wh produce plasma cells wh prod antibodies. These attack pathogens in plasma, lymph.

16. B & T lymphocytes perform a specific immune response in +,- 2 wks
The primary immune response: Recognition of a specific infection, ending in antibody production that eliminates said pathogen.

17. 5 types of immunoglobulins (antibodies)
igM: pentomers. Causes agglutination
igA: Dimers. From mucus membranes. Agglutinizing. In breast milk.
igD: Monomers on ‘naïve’ (not-yet specialized) B cells.
igG: Monomers, in blood, can pass to fetus giving it passive immunity.
igE: Monomers, from mast cells. Triggers allergic rxns.
What’s that spell!?
MADGE

18. Active immunity; from getting the disease or being immunized
Passive immunity is receiving the antibodies only. Temporary
Remember these???
What ‘er U lookin at!?

19. Smallpox vaccinations
Eradicated!
CDC & VECTOR

20. Immunology and the Rh factor
If an Rh – mother has an Rh + fetus:
Mother may develop memory immunity (sensitivity) to child’s Rh protein.
A subsequent Rh+ fetus could be attacked by Mom’s immune system

21. Organ transplants
Allergens as antigens: igE triggers mast cells to release histamines
Anaphylactic shock = loss of blood P
MS: T’s attack CNS
Type 1 Diabetes: attack pancreas
SCID; severe combined immune def.
AIDS attaches to the CD4 molec on the TH cells