1. SURFACE BARRIERS (EX: EXTERNAL BODY MEMBRANES)

2. INTERNAL DEFENSE (EX: CELLS, INFLAMATION, ANTIMICROBIAL PROTEINS, FEVER)

3. SPECIFIC IMMUNITY (EX: HUMORAL- ANTIBODY MEDIATED, CELL MEDIATED)

1. PHAGOCYTE BINDS TO MICROBE

2. PATHOGEN IS ENDOCYTOSED

3. PHAGOCYTIC VESICLE COMBINES WITH LYSOSOME

4. MICROBE DESTRUCTION AND DIGESTION

5. EXOCYTOSIS OF RESIDUAL BODY

PHAGOCYTE

(ROLE IN INTERNAL DEFENSE)

ENVELOPE AND DESTROY PATHOGENS

MACROPHAGES (TEMPORARY OR FIXED) DEVELOP AND RESIDE IN TISSUES

NEUTROPHILS ARE MOST ABUNDANT WBC's BECOME PHAGOCYTIC

EOSINOPHILS ARE WEAKLY PHAGOCYTIC AGAINST PARASITES

PERFORM IMMUNE SURVEILLANCE

DESTROY BY SIMULATING APOPTOSIS

ABLE TO RECOGNIZE AND DESTROY PATHOGENS SPECIFICALLY

INTERNAL DEFENSES

(PURPOSE, CARDIANL SIGNS, EVENTS)

PURPOSE: PREVENT, DISPOSE, CLEAR

CARDINAL SIGNS: HEAT, REDNESS, SWELLING, PAIN

EVENTS: CHEMICHAL RELEASE, VASODIALATION, EDEMA, PHAGOCYTIC MOBILIZAITON

HISTAMINE

CYTOKINES

KININS

PROTAGLANDINS

LEUKOTRIENES

COMPLEMENT

*ALL CAUSE VASODIALATION + OTHER THINGS*

INCREASED BLOOD FLOW TO AREA;

LEADS TO REDNESS AND HEAT

FLUID SEEPS INTO TISSUE SPACE CAUSING SWELLING

DILUTES TOXINS

DELIVERS HELPFUL INFLAMMATORY PROEITINS

PHAGOCYTIC MOBILIZATION

(WHAT ARE THE STEPS?)

1. LEUKOCYTOSIS

2. MARGINATION

3. DIAPEDESIS

4. CHEMOTAXIS

BLOOD FLOW SLOW AT INFLAMMED AREA

NEUTROPHILS ROLL ALONG CAPILARY ENDOTHELIAL CELLS WHICH INCORPORATE CELL ADHESION MOLECULES (CAMs)

NEUTROPHILS CLING TO WALL IN INFECTED AREA

INFLAMMATORY CHEMICHALS ACT AS "HOMING SIGNALS" ATTRACTING WBCs AND OTHER NEUTROPHILS

MONOCYTES FOLLOW AFTER NEUTROPHILS - DEVELOP INTO MACROPHAGES WITHIN 12 HOURS, REPLACING SHORT LIVED NEUTROPHILS

GENERALIZED ANTIVIRAL PROTEINS

...SECRETED BY CELLS SUCCUMBING TO VIRAL ATTACK AS A WARNING TO OTHERS

BLOCK DNA SYNTHESIS AND DEGRADE VIRAL RNA

ACTIVATE MACROPHAGES AND NK CELLS (ANTI-CANCEROUS EFFECT)

COMPLEMENT

(DEFINITION, ACTIVATION, FUNCTION)

DEFINITIONN: GROUP OF 20+ PLASMA PROTEINS CIRCULATING IN ACTIVE FORM; ENHANCE ADAPTIVE IMMUNITY

ACTIVATION: CLASSICAL PATHWAY- COMPLEMENT FIXATION- ANTIBODY BINDS TO PATHOGEN, C1 PROTEIN BIND TO ANTIBODY-PATHOGEN COMPLEX

-OR-

ALTERNATIVE PATHWAY- FACTORS B, D & P BIND TO POLYACCHARIDES ON PATHOGEN

*BOTH RESULT IN CLEAVAGE OF F3, C3a, C3b

FUNCTIONS: CELL LYSIS (C3b & MEMBRANE ATTACK COMPLEX [MAC]), PROMOTION OF PHAGOCYTOSIS (C3b), ENHANCED INFLAMMATION (C3a)

CHEMICHALS THAT RESET BODY'S HYPOTHALAMIC THERMOSTAT

PRODUCED BY LEUKOCYTES EXPOSED TO FOREIGN PROTEINS 

CAUSE SYSTEMIC RISE IN BODY TEMPS. 

1. ANTIBODY-MEDIATED IMMUNITY (A.K.A.- HUMORAL IMMUNITY) 

2. CCELL-MEDIATED IMMUNITY 

COMPLETE ANTIGEN

(IMMUNOGENICITY & REACTIVITY)

IMMUNOGENICITY: ABILITY TO STIMULATE LYMPHOCYTE PROLIFERATION AND ANTIBODY PRODUCTION

REACTIVITY: ABILITY TO REACT WITH IMMUNE PRODUCTS-- ACTIVATED LYMPHOCYTES AND ANTIBODIES 

A SMALL PEPTIDE 

REACTIVE BUT NOT IMMUNOGENIC 

CAUSES ALLERGIC REACTIONS 

ACTIVE SITES ON ANTIGEN THAT BIND WITH IMMUNE PRODUCTS 

*TYPICALLY MANY DIFFERENT ONES 

A COLLECTION OF SELF ANTIGEN GLYCOPROTEINS

TWO MAJOR GROUPS: 

1. CLASS 1 MHC

2. CLASS 2 MHC

ALL MHC PROTEINS HAVE A SURFACE GROOVE CONTAINING: 

1. PEPTIDE FROM PROTEIN BREAKDOWN IN HEALTHY CELLS

2. FRAGMENT OF FOREING PROTEIN IN INFECTED CELLS 

TISSUES WHERE LYMPHOCYTES BECOME...

IMMUNOCOMPETENT 

-OR-

SELF-TOLERANT

OCCURS IN BONE MARROW AND THYMUS 

WHERE IMMUNE CELLS CARRY OUT FUNTIONS 

OCCURS IN SPLEEN, LYMPH NODES, LYMPHOID FOLLICLES 

ANTIGEN PRESENTING CELLS (APCs)

(DEFINITION, TYPES, PURPOSE)

DEFINITION: CELLS THAT PHAGOCYTOSE ANTIGEN; ATTRACT THEM BY DISPLAYING A FRAGMENT OF ANTIGEN WITH MHC 2 PROTEINS

TYPES: DENDRITIC CELLS, LANGERHANS CELLS, MAGROPHAGES, B LYMPHOCYTES

PURPOSE: HELPS T LYMPHOCYTES RECOGNIZE ANTIGENS (THEY CANNOT DO SO ON THEIR OWN) 

ANTIBODY-MEDIATED RESPONSE 

(PRIMARY PARTICIPANT, MOST EFFECTIVE AGAINST) 

PRIMARY PARTICIPANT: B LYMPHOCYTES

*DIFFERENTIATE IN BONE MARROW AND LEAVE IT AS IMMUNOCOMPETENT BUT NAIVE B CELLS

MOST EFFECTIVE AGAINST: EXTRACELLUAR ANTIGEN 

(BACTERA, BACTERIAL TOXINS, FREE VIRUSES PRIOR TO CELLULAR INVATIONS) 

FIRST ENCOUNTER BETWEEN B CELL AND LEARNED ANTIGEN, USUALLY OCCURS IN SPLEEN OR LYMPH NODE

ANTIGEN BINDS TO SURFACE RECEPTORS ON B CELLS, STIMULATING COLONAL SELECITON

TRIGGERED BY ENDOCYTOSIS OF CROSS-LINKED RECEPTORS

THIS IS A RAPID PROLIFERATION OF IDENTICAL B CELLS 

MOST BECOME PLASMA CELLS- 90%

SOME BECOME MEMORY CELLS- 10%

B CELLS PRODUCED DURING CLONAL SELECTION

PRODUCING HUGE AMOUNT OF ANTIBODYS FOR 4-5 DAYS 

B CELLS CREATED DURING CLONAL SELECTION

INACTIVE DURING CURRENT INFECITON, THERE TO RESPOND TO SUBSEQUENT INFECITONS 

PRIMARY- INITIAL RESPONSE OF B CELLS

SECONDARY- IMMUNE RESPONSE TO SUBSEQUENT INFECITONS, FASTER, LONGER-LASTING, MORE INTENSE 

1. NATURAL ACTIVE

2. NATURAL PASSIVE

3. ATRIFICIAL ACTIVE

4. ARTIFICIAL PASSIVE