immune system non speciic to acquired

immunity

ability to resist/eliminate harmful foreign materials or abnormal cells

• defends agianst pathogens

• removes worn-out cells

• destroys abnormal/mutant cells

innate immunity (non-specific)

immune response

targets many pathogens

first line of defense

limited specificity

neutrophils, basophils, eosinophils

monocytes → macrophages

physical and chemical barriers of the innate immunity

skin + mucuous membranes

mechanical barriers (blocks entry)

acidic secretions (pH 3-5)

lysozyme (saliva) → destroys bacteria

mucus trap pathogens

Inflammation

isolate, destroy invaders

remove debris

prepare for healing

signs of inflammation

redness

heat

swelling

pain

process of inflammation

tissue damage → histamine release

vasodialtion → increase blood flow

increase in capillary permeability → fluid (exudate) enters tissue

swelling → pain

fibrin walls of area

cell movement

margination: cells stick to vessel walls

diapedesis: squeeze out of capillaries

positive chemotaxis: follow chemical signals

phagocyte response

leukocytosis: increase in WBC production

neutrophils arrive first 1-3 days

monocytes —> macrophages

opsonization

pathogens tagged by:

• antibodies

• complement proteins

killing mechanisms

phagocytosis

chemicals:

• nitric oxide

• lactoferrin

• histamine

• kinins

• pyrogens (fever)

Fever

caused by pyrogen

effects:

• increase in metabolic reactions

• decrease in bcaterial growth

• liver hides iron/zinc

Interferons

block viral replication

alpha/beta → innate

gamma → adaptive (activate macrophages)

NK (natural killer cells)

kill virus-infected and cancer cells

immediate, nonspecific

lyse membranes

complement system

~30 liver-produced plasma proteins

circulate inactive

Opsonization (C3B)

Inflammation (C3a,C5a)

Cell lysis → MAC (C5-C9)

punch holes in pathgoens → death

adaptive immunity (specific)

antigen specific

systemic

memory based

slower first response

B cells (humoral immunity)

produce antibodies

• antigen bings to the B-cel receptors

• Clonal expansion

  • plasma cells → antibodies

  • memory cells

IgM

first response

• binds + holds → done by plasma cells

pentamer = 10 ABS

powerful agglutination

IgG

strongers, most abundant

monomer

infection

IgA

found in secretions of the body

dimer = 4 ABS

IgD

attached to B-cell surface

B-cell receptor of activation for clonal selection

IgE

big

monomer

histamine release

allergies

what does PLAN stand for? (antibody functions)

Precipitation

Lysis

Agglutination

Neutralization

T cells (cell-mediated immunity)

Helper T (CD4) → activate immune cells

Cytotoxic T (CD8) → kill infected cells

• release perforins → kill target cell

regulatory T → suppress response

recognize antigen + MHC

MHC classes

Class I → all cells → CD8

Class II → APC → CD4

antigen presentation

dendritic cells and macrophages

process angtigen → present via MHC

activate T and B. cells

link innate + adaptive immunity

immunological memory

primary response

• lag: 3-6 days

• IgM first → then Igg

• slower, weaker

secondary response

• faster, stronger

• mostly IgG

• due to memory cells

acquired immunity types

natural active → infection

natural passive → mother to fetus

artificial active → vaccines

artificial passive → antibody injection

autoimmune disease

loss of self-tolerance

• multiple sclerosis

• rheumatoid arthritis

• type 1 diabetes

• lupus

Hypersensitivity

Immediate (IgE) → allergies, anaphylaxis

Subacute (IgG/IgM) —> immune complexes

Delayed (T-cell) → contact dermatitis