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IVP > Immunology, Inflammation & Repair > Flashcards

Immunology, Inflammation & Repair Flashcards

1
Q

What are the 5 pathological processes?

A
  1. Inflammation and Repair
  2. Degeneration & Cell Injury
  3. Circulatory Disturbances
  4. Disorders of Growth
  5. Accumulation of pigment and tissue deposits.
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2
Q

What kind of tissues can inflammation occur in?

A

LIVING tissue.

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3
Q

Inflammation is caused by cell damage, and/or exposure of a foreign agent. Cell damage might be caused by?

A
  1. Chemical agents
  2. Physical agents
  3. Infectious agents: Bacteria, fungi, viruses, protozoa, parasites
  4. Immune responses: Hypersensitivity and autoimmunity.
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4
Q

What are some innate defence mechanisms/ innate immuntiy?

A
  • Primarily inherited
  • not antigen-specific
  • Physical & physiological barriers
  • Host Chemicals e.g. cytokines, lysozyme
  • Host Cells e.g. phagocytes such as neutrophils
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5
Q

What is adaptive immunity

A
  • Recognition and response to a specific foreign antigen.
  • Chemicals e.g. cytokines
  • Host cells e.g. lymphocytes
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6
Q

What is pyogranulomatous inflammation?

A

active-chronic inflammation.
Combination of repair and continuing inflammation (innate and adaptive immunity). See chronic inflammation (macrophages, lymphocytes and plasma cells) as well as infiltration of polymorphonuclear cells (e.g. neutrophils)

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7
Q

What is aetiology?

A

The study of the causes of disease.

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8
Q

What are commensals?

A

Microbes that establish an inoffensive relationship with the host. Though alterations of HPEI may cause them to become pathogens and induce disease.

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9
Q

What is virulence?

A

Virulence refers to the relative pathogenicity of strains of microbes within a species.

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10
Q

The local manifestation of acute inflammation involves 3 parts of the INNATE inflammatory response:

A

1) haemodynamic changes
2) permeability changes
3) events involving leucocytes

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11
Q

What are the vascular changes of the innate response?

A

Oedema, redness, swelling, heat. These are non-specific but extremely rapid as they are mediated by chemicals already present in local tissues or cells,.

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12
Q

What is involved in initiation of acute inflammation (vascular and chemical innate response)?

A
  • Dying/ distressed cells release danger signal mediators = “alarmins” incl. heat-shock proteins, heparin sulphate and IL1a.
  • Sentinel cells already in the tissue, such as mast cells; occasional granulocytes; macrophages and DC’s; and respiratory , intestinal and urinary epithelial cells have internal and external TLRs which recognise PAMPS on the surface of pathogens.and incl. parts of bacterial/viral DNA and LPS
  • When TLRs of sentinel cells bind to PAMPS, or if the sentinel cell is exposed to alarmins from neighbouring cells, the cell releases pro-inflammatory cytokines (e.g. IL1, IL6 and TNF)
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13
Q

What are the mediators and mechanisms of the innate response?

A

Complex and interconnected mechanisms - 3 cascades (kinin, clotting and complement) and several other mediators.

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14
Q

What are the eicosanoids?

A

Prostaglandins and leukotrienes.
Prostaglandins are associated with pain from inflammation, can cause vasodilation and assist in vasc. permeability & oedema.
Leukotrienes produced by leucocytes is an inflammatory mediator and induces leucocyte chemotaxis, aggregation, adhesion, lysosomal enzyme release and superoxide anion generation.

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15
Q

What are the vasoactive amines?

A

Stored in the granules of tissue mast cells, basophils and platelets.
e.g. Histamine released from Mast cells. Increase vasc. permeability, assist in hypersensitivity reactions.

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16
Q

What are the vasoactive neuropeptides (tachykinins)?

A

Tachykinins are a group of neuropeptides that are released from peripheral and central nerves in response to a range of stimuli (tissue damage/pain). e.g. substance P

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17
Q

What are the building blocks for the cascades (kinin, clotting and complement)

A 
Acute phase proteins.
- Circulate in blood plasma or ECF
- Produced by liver
- increase production by cytokines
e.g. Fibrinogen - clotting 
C-reactive protein - Complement
Factor XII - Kinin & clotting
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18
Q

MEDIATORS & MECHANISMS:

What is the clotting cascade?

A

Initiated by tissue factor VII to VIIa (damaged tissue) OR by conversion of Factor XII to XIIa (exposed collagen, basement membrane).

  • Converts fibrinogen –> FIBRIN forming a fibrin clot,
  • Thrombin is also produced for its vasoactive properties.
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19
Q

MEDIATORS & MECHANISMS:

What is the kinin cascade?

A
  • Initiated by Factor XIIa
  • Produce BRADYKININ, induces pain, vas. dilation and vasc. permeability
  • Produces PLASMIN, which lyses fibrin (FEEDBACK LOOP for clotting cascade)
  • Plasmin also plays a role in activation of complement cascade.
  • release of histamine from mast cells & activate eicosanoid production.
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20
Q

MEDIATORS & MECHANISMS:

What is the complement cascade?

A
  • Series of interactive proteins e.g. C1, C2, …, C9 for the CLASSICAL pathway
    e. g. factor B, factor D, factor H, factor I and properdin (P) for the ALTERNATE pathway of activation.
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21
Q

Complement factors C5b+C6+C7+C8 make up a membrane attack complex that results in:

A

Membrane attack complex (MAC) –> cytolysis

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22
Q

What are some haemodynamic changes central to acute inflammation?

A
  • arteriolar dilation, transient vasoconstriction
  • Increased vol. of blood flow through the arterioles
  • Opening of additional capillary/venular beds (accommodate increased blood flow)
  • Congestion of the veins
  • Increased permeability of the microvasculature with the outpouring of fluid into the extravascular tissues.
  • results in conc. of RBC in the capillaries and venules
  • The conc. progresses, results in slowing or stasis of the blood flow in these small vessels
23
Q

What is a transudate?

A

A low protein fluid, ultrafiltrate of the blood plasma, consisting of water, small proteins and dissolved electrolytes. When present in ECM = oedema,

24
Q

What is an exudate?

A

An extravascular fluid with a high content of proteins, cellular debris and leucocytes and is usually the result of inflammation

25
Q

What comprises the cellular innate response?

A
  • Events involving leucocytes.

- Margination, adhesion and migration

26
Q

What is margination?

A

With inflammation, more leucocytes come into contact with the vessel walls due to haemodynamic changes (vasodilation) resulting in slowing of blood flow. Cells may roll along capillary walls and momentarily stop.
- Adhesion molecules on the surface of leucocytes and endothelial cells are also involved.

27
Q

What are polymorphonuclear cells?

A

GRANULOCYTES:

  • Neutrophils
  • Basophils
  • Eosinophils
28
Q

What are the mononuclear cells?

A
  • Lymphocytes
  • Plasma cells
  • Macrophages/ mast cells
29
Q

What are neutrophils?

A

Granulocytes that target bacteria

  • Myelopoiesis
  • 1 day in circulation
  • 1-2 days in tissue
  • Death
  • Once in tissue do not reenter blood
  • Kill bacteria > enzymes called lysosomes > form phagolysosomes > attack and digestion by granular contents.
30
Q

What are eosinophils?

A

Granulocytes that target allergies, parasites & fungal agents

  • Myelopoiesis
  • cytoplasmic granules with affinity for eosin dye
  • De-granulate in response to large foreign materials that are unable to be phagocytosed
  • can cause histamine release from mast cells
  • Important in Type I hypersensitivity
31
Q

What are Basophils?

A

Granulocytes

  • Myelopoiesis
  • Blue staining granules contain heparin, histamine and proteinases
  • Similar morphology to neutrophils (bilobed nucleus, granules blue/purple)
  • Chemotaxis –> bind to IgE –> Degranulation
32
Q

What are Mast cells?

A

Respond to immunologic or allergic reactions

  • Blue staining cytoplasmic granules
  • Found throughout body
  • BM origin –> circulate in blood (unrecognisable cells) –> tissues (differentiate to mast cells)
  • Recruit eosinophils to tissues via chemotaxins
33
Q

What are Monocytes?

A
  • BM origin
  • Released into circulatory blood –> migrate to tissues (Macrophages)
  • a small proportion of macrophages originate from proliferation of other macrophages resident in tissues (“histiocytes”).
34
Q

What are Macrophages?

A
  • 2 types: Tissue (histiocytes) & Monocytes.
  • Abundant cytoplasm
  • large nuclei of variable shape
  • arrive at site of inflammation after first wave of neutrophils
  • last up to weeks
  • large numbers in chronic inflammation
  • Phagocytose and kill microbes
  • recruit other leucocytes,
  • Clean up cellular debris
  • Synthesise cytokines - IL1, TNF
35
Q

What does the presence of mononuclear cells usually indicate?

A

Chronic disease

36
Q

What are NK cells?

A

Natural killer cells are lymphocytes (~15% of lymphocyte population)

  • Activated by PAMPS
  • Produce cytokines (IL-4, IFNg) - directing immune responses in the tissues and providing further activation of macrophages & NK cells
  • No memory
  • Non-specific
  • Kill neoplastic and Infected cells
37
Q

What are B cells?

A
  • Produce IgM
  • can be partially activated
  • NO memory
  • Multiple IgM binding sites: good at agglutinating bacteria and antigens –> phagocytosis
  • Antigen-IgM complexes activate the complement cascade
38
Q

What comprises the Adaptive immune response?

A
  • Lymphocytes
  • Plasma cells
  • accumulation of macrophages

It is antigen specific. Produces memory, antigen presenting cells & co-infammatory signals. MHCI & MHCII.

39
Q

What are lymphocytes?

A
  • smaller than neutrophils,
  • Ovoid, non-lobulated, densely stained nucleus
  • Scant cytoplasm
  • Usually appear later in inflammatory response (except NK)
  • Produced by PRIMARY lymphoid organs (BM and Thymus)
  • Migrate to SECONDARY lymphoid organs (spleen & lymph nodes)
  • re-circulate between lymphoid tissue, blood & lymphatics
40
Q

What cells are MHCI expressed by? and what is its role?

A

ALL cells. MHCI is responsible for presentation of ENDOGENOUS antigens (ie antigens present within the cytoplasm of cells)

41
Q

MHCI only interacts with cells expressing CD8. Where is CD8 found?

A

CD8 is a molecule only expressed in Tc cells and some Ts cells (or T reg).
Tc cells are antigen specific and kill by inducing apoptosis (similar to NK)

42
Q

Tc cells need activation and proliferation: co-stimulation by Th1 cells

A
  • naive Tc cells sit in lymphoid tissues such as lymph nodes where they are exposed to DCs, then they travel to lymph nodes and present it on MHC1 to naive Tc cells.
43
Q

How do Tc cells differ from NK cells

A

They both induce apoptosis. But Tc cells are antigen specific and must undergo a period of activation & proliferation before they can kill infected/neoplastic cells.

44
Q

Tc cells can only be activated & undergo proliferation if stimulated by ALL 3 of the following:

A

1) Presentation of antigen on MHCI
2) IL12 from the activated DC
3) IL2 and IFNg from an adjacent T helper 1 cell

45
Q

What is the role of MHCII in presenting exogenous antigens to the immune system?

A

Th cells are CD4+ and receive antigen on MHCII.

  • MHCII is present ONLY on professional antigen-presenting cells e.g. DCs, macrophagesm B cels and some mucosal cells stimulated by IFNg.
  • It only interacts with CD4 on Th cells (not CD8 on Tc cells)
  • It presents EXOGENOUS antigen: phagocytosed>processed with lysosome>loaded onto MHCII>surface of cell.
46
Q

What do Th1 cells do?

A

T helper 1 cells activate and direct Tc cells in CELLULAR immunity

47
Q

What do Th2 cells do?

A

T helper 2 cells direct the ADAPTIVE response. The main characteristics are to do with ANTBODY-based immunity, repair and resolution.
- Bcells proliferate and transform to plasma cells and then produce antibody classes IgG, IgA and IgE.

48
Q

What are antibodies?

A

A form of immunoglobulin that is soluble.
It is a large Y-shape protein produced by plasma cells that is used by the immune system to identify and neutralize foreign objects.

49
Q

Where is IgG produced and what is its function?

A
  • Secreted by plasma cells in lymph nodes, spleen and bone marrow.
  • Most common Ig in plasma
  • In tissues, binds to specific antigen - neutralises, opsonises or forms Ag-Ab complexes that fix complement.
50
Q

Where is IgA produced and what is its function?

A
  • Secreted from mucosal surfaces & neutralises & agglutinates pathogens.
51
Q

Where is IgE produced and what is its function?

A
  • Made by plasma cells under surfaces
  • Fits a receptor on the surface of mast cells and basophils
  • when IgE on the surface of a mast cell contacts its antigen –> mast cell degranulates, releases histamine.
    Developed for eliminating intestinal worms or irritants.
  • When inappropriate results in Type 1 hypersensitivity (allergy, anaphylaxis, eosinophilic granuloma)
52
Q

Where is IgD found

A
  • functions as a receptor on the surface of Bcells

- not found in all species

53
Q

Where is IgM produced and what is its function?

A
  • IgM is a pentamer (10 binding sites)
  • effective at agglutinating pathogens, forming Ag-Ab complexes to fix complement, neutralising and opsonising.
  • It is mostly produced by plasma cells (originate from B2 cells) in the lymphoid tissues as the initial phase of the adaptive response.
54
Q

What immunoglobulins can all form (immune) Ag-Ab complexes?

A

IgG, IgA and IgM.

If excessive, or become deposited in tissue, they cause of local fixation of complement and activation of macrophages and neutrophils which cause inflammatory disease.

IVP (3 decks)

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