Immunity and Inflammation Flashcards
1
Q
Barriers: 1st line of defense
A
- Physical/Mechanical: Intact skin/sloughing of skin, mucus, cilia, coughing, and sneezing, tears, etc.
- Chemical: Skin secretions > acid pH, hair follicles > sebum, tears, saliva > lysozyme, stomach > hydrochloric acid, enzymes
2
Q
Barriers: 2nd and 3rd line of defense
A
- When barriers breached, innate immune system kicks in
- Adaptive immune system
3
Q
Lymphoid system
A
- Responsible for immunological defense of body: self/non-self recognition, protection from foreign invader, handles by B cells, T cells, and APCs -> initiate and participate in innate immune response
- Component organs: lymph node, thymus, and spleen and diffuse lymphoid tissue
4
Q
Lymphatic tissue
A
- Mucosa associated lymphoid tissue(MALT)
- Gut associated lymphatic tissue
- Peyer’s patches
- Bronchus associated lymphatic tissue(BALT)
- Located in walls of bronchus
- Appendix, tonsils
- Located in walls of bronchus
5
Q
Lymphoid organs
A
- Primary lymphoid organ
- Developmental and maturation of lymphocytes -> immunocompetent cells- Thymus, fetal liver, pre/post natal bone marrow
- Secondary lymphoid organs
- Provide proper environment for immunocompetent cells to react
- Lymph node, spleen, diffuse lymphoid tissue, and post-natal bone marrow
6
Q
Thymus
A
- Located in superior mediastinum and extending over greater vessels of heart
- Encapsulated organ with two lobes
- Originates early in the embryo and continue to grow until puberty. after first few years, it begin to atrophy and becomes infiltrated with adipocytes
- During development of embryo, T-cells migrate to thymus to become immunologically competent
- 2 major components:
- Parenchyma(cellular component)
- Stroma(supporting connective tissue) - Encapsulated connective tissue and sends septa into lobes, subdividing them into incomplete lobes
7
Q
Thymus cortex
A
- Dense population of lymphocytes compared to medulla region of thymus. Mainly T-cells -> extensive proliferation and becomes immunocompetent
- Contains macrophages and epithelial reticular cells(ERC or TEC: 3 types in cortex and 3 types in medulla)
- ERC function include barrier formation(occluding junctions) and some types help educate T-cells
8
Q
Type 1: ERC
A
- Separates the capsule and septa from cortex
- Surrounds the vascular elements of cortex
- Forms the blood - thymus barrier
- Isolates the thymus cortex from rest of body
- Polymorphous nuclei and a well defined nucleous
9
Q
Type 2 ERC and Type 3 ERC
A
- Type 2:
- located in mid cortex
- have long wide processes that form desmosomal junctions with each other which further subdivides cortex into small T cell compartments, large pale nucleus, no nucleous
Type 3 ERC: - Deep in cortex near medulla, corticomedullary junction
- Long-wide processes similar to Type 1, compartments more T-cells
10
Q
Thymus Cortex ERCs
A
- Type 2 and 3 play a role in education of T-cells, presents self-antigens, MHC 1 and 2 molecules to developing cells
- Thymus is very compartmentalized organ. Prevents T-cells from getting in contact with any foreign antigen
- T-cells(competent but naive) enter medulla of thymus for distribution to secondary lymphatic organs around body
11
Q
Thymus summary
A
- Type 2 and 3 ERCs educate T-cells by testing ability to recognize self-MHC molecules and self-epitopes
- T-cells not able to recognize self-MHC moelcules and auto-reactive thymocytes are destroyed
- Highly compartmentalized
12
Q
Innate immunity
A
- Secondary system of host defense
- Always present
- Immediate defense
- Responses generic
- Short-lived immunity
13
Q
Type of cells involved
A
- Mast cells: release bioactive chemicals
- Neutrophils: signals other cells, eats and digests pathogens
- Macrophages: stimulates other immune cells and eats/digests pathogens and cellular debris
14
Q
PAMPs
A
- LPS
- Flagellin
- Lipoteichoic acids
- Peptidoglycan
- ds/ss vRNA, bacterial DNA
- Repeating structural units
15
Q
Pattern Recognition Receptors
A
- 4 major classes: 2 membrane-bound and 2 cytosolic
- C-type lectin receptors(CLRs) bind to mannose, fucose or glycan carbohydrates
- Toll-like receptors: 13 different types. TLR-2 and TLR-4 binds LPS, TLR-3 binds dsRNA, TLR-5 binds flagellin
- NOD-like(nucleotide-binding and oligomerization domain) receptors binds MAMPs(viralRNA, sp toxins strep and listeria sp) -> pro inflammatory cytokines
- RIG1-Like Receptors(retinoic acid inducible genes) binds viral RNA -> interferon and other anti-viral cytokines
16
Q
Acute Inflammation
A
- Involves changes that occur within minutes of injury and persist for several hours or days
- Self-limiting process whose goal is total/partial elimination of injury with restoration of damaged tissue within days of the injury
- Vascular response to injury is a reactionary process that sets up delivery system of inflammation
17
Q
5 signs of acute inflammation
A
- Rubor: redness
- Tumor: swelling
- Calor: heat
- Dolor: pain
- Functio laesa: loss of function
- Redness and heat results from increase in blood volume(vasodilation), swelling results from changes in vascular permeability leading to fluid exudation, plasma proteins, and WBCs
18
Q
Repair and Healing
A
- One of the primary functions of inflammation process is to heal wounded tissue
- Resolution involves return of injured tissue to normal structure and function. Occurs when injury was not extensive and parenchyma are capable of regenerating. Alternative is fibrous repair
19
Q
Fibrous Repair
A
- Cut in skin -> bleeding -> formation of clot
- Acute inflammation develops:
- Rapid accumulation of neutrophil followed by macrophages
- Macrophages responsible for wound debridement, removal of any RBCs, fibrin and cellular debris making room for capillary buds and fibriblast
- Capillary budding from endothelial cells from pre-existing capil project out and form capillary loops -> forms arterioles and venules
- Fibroblast enter and remodel fibrin-fibronectin matrix into scar tissue
- New arterioles and venules, replacement of skin if needed
- Granulation: process by which initial blood clot converted into fibrous connective tissues
- Clot replaced by granulation tissue, characterized by proliferation of new small blood vessels and fibroblasts- Derived from pink, soft granular appearance on surface of wound
20
Q
Adaptive immunity
A
- Tertiary source of host defense
- Called into action - cell mediated and humoral immunity
- Takes time to mount defense
- Responses are antigen specific
- Remembers specific pathogens
21
Q
Antigens and Antibodies
A
- Antigen: foreign body; eptiope - region that reacts with an antibody. TCR, SIGs
- Antibodies: immunoglobulin, marks antigens for elimination
22
Q
Types of immunoglobulins
A
- IgM: stops infection by toxins and viruses
- IgG: protects newborns
- IgA: defense of mucosal surfaces
- IgE: allergites
- IgD: triggers B lymphocytes
23
Q
Immunological specificity and memory
A
- Recognition of specific invader(MHC(HLA)):
- Antigen enters dendritic cell
- Enzyme inside cell breaks antigen to pieces
- Antigen pieces bind to MHC protein inside ER
- MHC antigen complex transported to cell surface
- MHC protein presents antigen on surface of cell membrane
24
Q
Types of cells involved
A
- Macrophages: engulf foreign bodies
- Helper T cells: boost immune response
- Cytotoxic: eliminates infected or neoplastic cells
- B cells: produces antibodies
25
Cell mediated
- Macrophages
- Effector Helper T-cells: interleukins
- Effector cytotoxic T-cells: perforans
Process:
- MHC marker on pathogen binds to antigen-MHC complex
- Binds antigen-MHC receptor on helper T cells -> memory cytotoxic T cell -> differentiation to effector cytotoxic T cell
26
Antibody-Mediated
- B cells
- Effector B-cells
- Humoral immue response
Process: antigen bind to antigen-MHC complex -> helper T cell activate memory B cell -> differentiation and mitosis -> populations of effector and memory B cells
27
Immune system disorders
- Autoimmunity: immune system attacks self cells
- Hypersensitivies: immune system overreacts
- Immodeficiencies: immune system under reacts
28
Autoimmunity
- T cells are "bored" -> go do something
- Tissue/organ specific and non-specific
- Arthritis, Crohn's disease
29
Hypersensitivies
- Immediate
- Cytotoxic
- Immune complex
- Delayed: tuberculosis
30
Immediate Hypersensitivity
- APC interactions -> helper T cell activate B cell -> make IgE -> mast celll binding -> releases allergic mediators(histamine, serotonin, etc.) -> allergies
31
Allergies
- First time allergy prone person runs across allergen -> production of large amount of allergen IgE antibody
- These IgE molecules attach themselves to mast cells
- Second exposure -> IgE primed mast cells release chemicals -> allergy symptoms
32
Delayed type hypersensitivity
- Cell mediated hypersensitivity characterized by tissue damage due to inflammatory responses produced by TH1 inflammatory cells -> release cytokines
- Symptoms appear several hours following secondary exposure to eliciting antigens
- Typical antigens include microbes, self-antigens, chemicals that covalently bind to skin creating new antigens(contact dermatitis)
