Ch 21 - Body defense Flashcards
types of hemocytoblasts (WBC’s) involved in NON-SPECIFIC defence (can attack anything)
Basophils, Eosinophils, Neutrophils, Monocytes (=macrophages)
type of hemocytoblast (WBC) involved in SPECIFIC defence
lymphocyte that form 3 major types
T and B cells attack specific antigens
‘natural killer’ lymphocytes are NON-specific and involved in 1st line of defense
some WBC’s develop further into these
monocytes to macrophages = carry out phagocytosis
B lymphocytes to plasma cells = produce antibodies
2 ways a foreign organism can be destroyed
Phagocytosis - engulfed by neutrophil/macrophage
Lysis - cell membrane attacked and ruptured
the two intrinsic defence systems of the immune system
INNATE (Non-specific) - what you are born with and are active against any sort of invader
ADAPTIVE (Specific) - what develops after birth when exposed to antigens.
Both work together to get job done! neither one works alone
two types of 1st line of defines. Innate (non-specific) defence against any type of foreign material or antigens
Surface barriers - skin (keratin resists compromising), mucosal membranes (internal organs)
Chemical barriers - skin (slightly acidic, inhibit bacterial growth), HCl and enzymes in stomach, saliva and tears, mucus (traps organisms)
Types of second line of defense
Phagocytosis - engulf and destroy antigens
Lysis by Natural Killer cells (T-cells)
inflammation - Redness / Heat / Swelling / Pain (sometimes impairment)
Antimicrobial Proteins - enhance defense, attack directly and hinder antigen ability to reproduce
3 types of WBC’s involved in Phagocytosis
Macrophages - “heavy hitters” that repeatedly kill and also release ‘respiratory burst’ of oxidizing chemicals to kill antigens. Free (wander through tissues) and Fixed (stay in place)
Neutrophils - most common first responders to infection. they are destroyed during attack on invaders (suicide killer)
Eosinophils - weak phagocytes - surround parasites and release enzymes to attack
explain the process of phagocyte mobilization (EXAM)
- Leukocytes stimulate and induce
- Margination (pavementing) - WBC’s move along capillaries and cling to CAM’s
- CAM’s (cell adhesion molecules) - mark the cite of damage/infection
- Diapedesis - WBC’s squeeze between cells and move toward the injury (by amoeboid motion)
- Positive chemotaxis - WBC’s follow increasing concentration to injury
- Neutrophils are 1st responders, then monocytes which convert to macrophages
Mechanism (process) of Phagocytosis (EXAM)
- adherence to phagocyte to pathogen
- engulfing into phagosome
- fusion with lysosome
- hydrolysis/internal digestion by enzymes
- killing by burst of free radicals or oxidizing chemicals
- killing by defensins (in neutrophils)
- exocytosis of the remaining residual body (removal)
results of phagocytosis (what do you see?)
Pus - evidence that the phagocytic cells are working
Abscess - infection not cleared and walled off by collagen fibers
Lysis by natural killer (NK) cells
- large granular T-lymphocyte involved in non-specific defines.
- found in blood, lymph vessels and other tissues and crawl/look for abnormal marker proteins
- kill cells (& cancer cells) by secreting perforin and granzymes
perforin: perforates into cell and forms pores
granzymes: enter through pores and attack membrane leading to apoptosis (natural cell death/degeneration)
NOTE: NK cells also help stimulate inflammatory response
Inflammation response
triggered whenever injury/infection and prevents spread of pathogens while it prepares for repair.
4 cardinal signs: (RHSP) Redness, Heat, Swelling, Pain (and sometimes impairment)
stimulus that triggers inflammatory response
- histamine released by mast cells in loose connective tissue is the ‘early warning system’
- Toll-like receptors (TLR’s) on macrophages recognize microbes and trigger the release of cytokines (chemical messenger)
- Kinins, prostaglandins, leukotrienes, complement - are released by injured tissues. phagocytes, lymphocytes, basophils all can trigger the process of inflammatory response
Process of the inflammatory response
- inflammatory chemicals released into extracellular fluid
- triggers dilation of arterioles - increase blood flow - REDNESS and HEAT
- increased permeability of capillaries (SWELLING and PAIN)
- release of exudate (fluid) that dilutes harmful substances and aids healing by bringing more nutrients
- damaged area walled off for repair
- foreign materials moved/swept into lymphatic vessels
- More PAIN from toxins and decreased nutrients in area (prostaglandins and kinins)
- damage to mucosa - secretion of defensins increased
- All this facilitates destruction of invaders and repairs damaged tiisues
Role of antimicrobial proteins
enhance defence and attack microorganisms directly
two types of proteins: Interferons and Complement
Interferon proteins
Produced by cells infected with viruses
non specific protein that acts against a range of viruses that prevents the spread to other cells by preventing synthesis
Activates macrophages and Natural Killer (non-specific T-cells) to attack cancer and infected cells thus reducing inflammation.
Note: genetically engineered interferons are used to treat genital warts, Hep C, and viral infection from transplants
Complement proteins
20+ inactive plasma proteins that act in a cascade (circulate)
Assist in Specific and Non-Specific defence and destroys foreign antigens
TWO Pathways: CLASSICAL (bind to C1 antibody complex). and ALTERNATIVE (exposure to cell wall)
Both pathways lead to formation of C3 - cleavage (split) into C3a/C3b causes cell LYSIS, enhance phagocytosis, inflammation and production of C proteins.
Cleavage of C3 into C3A and C3B
- Lysis of infected cells - C3B binds to target cell and inserts a (MAC) membrane attack complex = rupture
- Opsonization - aids phagocytosis - C3B coats microorganism with protein so phagocytes can attack easily
- Stimulates Inflammation - C3A stimulate mast cells and basophils to release inflammatory chemicals to attract other cells to area
- C reactive Protein - production of C proteins in the liver is stimulated and targets invaders for phagocytosis
Function of FEVER
thermostat in hypothalamus reset in response to pyrogens from WBC’s and macrophages
too high is bad but a moderate increase benefits that inhibit bacterial growth and speeds up repair
-causes the liver and spleen to bind up iron and zinc needed for multiplication
-Increases metabolic rate = speeds up repair
