The yellow text is for extra

information – no need to copy

down

First Line of DefenseFirst Line of Defense

Skin & mucous membranesPhysical barrierChemical barrier

○Lower pH○ “Flushing” of invades (tears, sweat,

mucus)○Antimicrobial proteins (lysozymes)

Digest cell walls

Second Line of Second Line of DefenseDefense Non-specific Phagocytic leukocytes (WBC)

Neutrophils (60-70%)○Attracted to chemical signals from

damaged cells (chemotaxis)○Engulf & destroy microbes

Second Line of Second Line of DefenseDefense

Monocytes (5%)○Develop into

long-lasting microphagesAttach to polysaccharides on

microbe’s surface○Some migrate, some are permanent

in lungs, liver, kidneys, brain, connective tissues, lymph nodes, & spleen

Second Line of Second Line of DefenseDefense

Eosinophils (1.5%)○Defend against larger parasitic

invadersNatural killer cells (NK)

○Destroy virus-infected body cells

Second Line of Second Line of DefenseDefense The Inflammatory Response

Precapillary arterioles dilatePostcapillary venules constrict

○ Inc. blood supply (redness & heat)○Pushes fluid out (edema)

Second Line of Second Line of DefenseDefense

Initiated by chemical signals○Histamine

Produced by basophils (type of WBC) and mast cells in connective tissue

Increase dilation

○ProstaglandinsPromote blood flow to injury siteBoth inc. addition of clotting factors to the

area for healing

Second Line of Second Line of DefenseDefense

Phagocytic cells attracted to area by chemokines (secreted by blood vessel endothelial cells & monocytes)

Pyrogens○Released by leukocytes○Raise body temp○ Inhibit growth & facilitate

phagocytosis

Third Line of DefenseThird Line of Defense Specific Immunity

Lymphocytes○B cells & T cells○ In spleen, lymph nodes, & lymphatic

tissues○Detect specific antigens

Foreign molecules that elicit specific response

○Activate & produce certain antibodies○Have membrane antigen receptors

Third Line of DefenseThird Line of Defense

○During early development, B cell or T cell develops receptors for any type of antigen (before contact)

○When contact with antigen, lymphocyte divides, differentiates, forming two clonesEffector cells (B cells secrete

antibody)Memory cells (long-living; have

receptors for antigen)

Third Line of DefenseThird Line of Defense First contact – primary immune

response Second contact – secondary I.R.

Quicker (due to memory)Larger

scale

Lymphocyte Lymphocyte DevelopmentDevelopment

From pluripotent stem cellsFetal bone marrow & liverIf then move to thymus T cell

If stays in bone marrow B cell

Key: self vs non-selfIf not, apoptosis

Major Major Histocompatibility Histocompatibility

Complex (MHC)Complex (MHC) Cell surface glycoproteins Mark body cells as “self” Class I: on all nucleated cells Class II: specialized (macrophages &

B cells) Known as Antigen Presenting

Complex (APC)

Major Major Histocompatibility Histocompatibility

Complex (MHC)Complex (MHC) Very polymorphicMakes almost all people unique

When infection, MHC presents antigen to T cell to alert them (antigen presentation)

Class I present to cytotoxic T cells (TC)

Class II present to helper T cells (TH)

Immune ResponseImmune Response

Humoral ImmunityB cell activationDefend free invaders in body fluid

Immune ResponseImmune Response Cell-mediated immunity

T cell activationWhen cytotoxic T cell activated by

Class I MHC, becomes active killer○Kills target cell with perforin

Protein that forms pores in target cell membrane

Antibody-Mediated Antibody-Mediated DisposalDisposal 1) Neutralization

Antibody binds to & blocks antigen activity

2) OpsonizationBound antibodies enhance

macrophage attachment to the microbes

3) AgglutinationClumping of microbes

Antibody-Mediated Antibody-Mediated DisposalDisposal

4) PrecipitationCross-linking of soluble antigens to

form immobile precipitate 5) Complement fixation

Activation of complement system○20 proteins inactive when no

infection○When infected, cascade of

activation starts○End result – lysis

Plant Immune Plant Immune SystemSystem Plant defenses include molecular

recognition systems with systemic responses

Infection triggers chemical responsesDestroy infected and

adjacent cells, thus localizing the effects.

Immunity Immunity ApplicationsApplications Active immunity

Achieved by exposure & recovery or vaccination

Passive immunityReceiving antibodies

Blood CompatibilityBased on surface antigen of RBC

Immunity Immunity ApplicationsApplications Rh factor

RBC antigen (IgG)Mom Rh-, fetus Rh+

○Mother may have a T-dependent humoral responseAffects subsequent pregnancies

-Memory cells produce IgG

Immunity Immunity ApplicationsApplications Tissues & Organs

MHC can cause rejection Allergies

Exaggerated responses to envi. antigens

Tend to involve IgE & mast cellsRelease of histamineCan result in abrupt dilation of blood

vessls, lowering bp (anaphylactic shock)

Immunity Immunity ApplicationsApplications Autoimmune Diseases

Turns against itselfLupus, MS, diabetes, rheumatoid

arthritis

Immunity Immunity ApplicationsApplications SCID

Both humoral & cell-mediated problems

Hodgkin’s disease○Damages lymphatic system

Immunity Immunity ApplicationsApplications AIDS

Caused by HIVHIV-1 (more virulent strain) & HIV-2Both infect cells that have surface

CD4 moleculesCan also infect helper T cells,

B lymphocytes, & brain cells

Immunity Immunity ApplicationsApplications

Entry of virus requires CD4 & a coreceptor protein○Fusin (CXCR4), found on helper T

cells○CCR5, found on macrophages

Integrates into genomeBody makes HIV antibodies intially

Immunity Immunity ApplicationsApplications

Over time, viral load increasesHelper T cells become infected &

dieUse DNA-synthesis inhibitors,

reverse transcriptase inhibitors, & protease inhibitors to combat