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Pathology-1 > Immunopathology I > Flashcards

Immunopathology I Flashcards

1
Q

Components of the Innate immune system

A

epithelial barriers, Macrophages, neutrophils, NKC, complement system, histiocytes

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2
Q

What are the branches of the Adaptive immune system

A
  1. Cell mediated immunity
    - APCs

CD4Tcell

CD8 Tcell

  1. Antibody mediated
    - Bcells
    - AB
    - Complement
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3
Q

Acquired immunity: cell mediated

A

“immature” DC encounter antigen–>migrate to paracortical area LN–>present to T cell–> activate either CD8 (MHCI) or CD4 (MHCII).

CD4Tcel–> proliferation of Bcells, MO, Neutrophils

CD8Tcell–> directly attack infected cells causing their lysis

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4
Q

Acquired Immunity: antibody mediated

A

SC–>immature B cell–>Mature B cell + Antigen–>1. immunoblasts or initiate the formation of a 2. germinal center

  1. Immunoblasts (IgM)–> Plasmacytoid
    - –>Plasma cell (IgG, IgA, IgE)
  2. germinal center, mature b cells duplicate/clonal expansion–>centroblasts

–>somatic mutations within Ig variable region–>

a. Centrocytes (- selection=apoptosis)
- b. Centrocytes (+selection due to BCR affinity for anti.)–> Heavy chain class switching–>B cells leave germinal center and diferentiation into
- memomy B cells or plamsma cells (IgG, IgA, IgE)

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5
Q

Pre germinal B cells will produce what Ig?

A

IgD, IgM

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6
Q

Post germinal B cells produce IgM and IgD

A
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7
Q

How does complement aid in the antibody mediated response?

A

complement will opsonize the antigen/antibody complex thus marking it for phagocytosis by MO

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8
Q

Summary slide of innate and adaptive immune response

A
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9
Q

Maturation of T cells

A
  1. T cell born in the bone marrow–>mature in thymus–>Here they are - for TCR, CD3, CD4, CD8
  2. within the cortex of the thymus T cells acquire TCR, CD3 and become +CD4/CD8
  3. Positive and negative selection of T cells occur and thus eliminate self reactive T cells
  4. T cells mature in the medulla of the thymus and become either CD4+ or CD8+.
  5. Exit thymus and enter the peripheral circulation or the paracortical area of the LN
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10
Q

What is the histocompatibility complex?

A
  • highly polymorphic system with unique alleles inherited that are clustered on a -small segment of chr 6.
  • They bind peptide fragments of foreign proteins for presentation to T cells as T cells (in contrast to B cells) can only recognize membrane-bound antigens
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11
Q

Class I MHC

A

from HLA, B,C,

  • Present on all nucleated cells & platelets
  • linked to B-2 Microglobin
  • present antigen to CD8+ lymphoctes
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12
Q

Class II MHC

A

from HLA- DR, DQ, DP

  • restricted to APCs
  • present extracellular antigen that is first internalized and processed
  • present antigen to CD4+
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13
Q

Class III MHC

A

encodes components of the complement system

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14
Q

TCR complex

A
  1. TCR alpha/Beta are linked to the CD3 complex and zeta chains
  2. MHC displayed on the APCs recognized by TCR
  3. 1st signal of activation-Microbe activates APC–>MHC+TCR associated zeta chains and CD3

2nd signal- B7 proteins (APC) and recognize CD28 (T-cells)

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15
Q

What are cytokines?

A

short acting soluble mediators that regulate the interaction among many different cells (lymphocytes, inflammatory cells, endothelial cells, etc.)

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16
Q

Cytokines that regulate lymphocyte growth?

A

IL-2, IL-4, IL-12, TGF

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17
Q

Cytokines that mediate innate immunity?

A

IL-1, TNF, IL-6

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18
Q

Cytokines that stimulate hematopoiesis?

A

G-CSF

GM-CSF

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19
Q

cytokines that attract leukocytes?

A

chemokines

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20
Q

cytokines that activate inflammatory cells?

A
  • IFN-gamma
  • IL-5
  • TNF
  • Lymphotoxin
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21
Q

What are Type I Hypersensitity rxns?

A

Anaphylactic Type

-systemic anaphylaxis, Atopic dermatitis, Asthma

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22
Q

What antibody mediates Type I HSR?

A

IgE

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23
Q

What cells are involved in T1 HSR?

A

mast cells, eosinophils, complement

24
Q

What are the primary and secondary mediators in T1 HSR?

A

Primary- Preformed granule contents in effector cells (histamine, proteases, proteoglycans)

Secondary - Synthesized and released lipid derived (leukotrines, prostaglandins) and cytokines (TNF, Chemokines, IL-1)

25
Q

Mechanism of T1 HSR

A

parastie presented on DC

  1. CD4 TH2–>IL-3 & 5–>eosinophil–>release granules & later deposition in tissues.
  2. CD4 TH2–>IL-4 & 13–> B cells–> IgE & sustain production of TH-2 cells
    - IgE induces powerful mediators from mast cells: histamine, leukotrienes, heparin, prostaglandin, & chemokines
26
Q

Type II Hypersensitivity Reactions directed against?

A

mediated by AB, against cell surface antigens or extracellular matrix

27
Q

What are 3 mechanisms in TII HSR?

A
  1. opsonization & complement-mediated phagocytosis
  2. complement-mediated inflammation

*when Ab deposit in EC tissue, the activated complement, which recruits neutrophils and monocytes causing injury by inflammatoin

  1. Ab mediated cellular dysfunction

*anti-R antibodies impair or dysregulate the function of the receptors without causing cell injury or inflammation

28
Q

What causes TII HSR: Opsonization and phagocytosis?

A
  • transfusion reactions
  • Rh Incompatibility
  • Autoimmune hemolytic anemia
  • certain drug rxns
29
Q

What causes TII HSR: complement-mediated inflammation?

A
  • glomerulonephritis
  • vascular rejection in organ graphs
30
Q

What are the causes of Type II HSR?

A

Myasthenia gravis

graves disease

31
Q

What is Type III hypersensitivity reactions?

A

antigen-antibody complexes produce tissue damage by initiating inflammation at sites of deposition, typically vessel wall

*IgM and IgG bind antigens in circulation and complexes deposit in tissues–>inflammation

*recruit leukocytes which do the actual damage

32
Q

What are examples of local Type III HSR?

A
  • post-streptococcal glomerulonephritis
  • arthus reactions
33
Q

What are examples of systemic Type III HSR?

A
  • systemic lupus erythematosis (SLE)
  • polyarteritis nodosa
  • Serum sickness
34
Q

What type of Hypersensitivity reaction is this?

A

Type III

  • immune complex vasculities
  • losts lymphocytes=cell mediated process
  • thickened wall the B cell process
35
Q

How are Type IV Hypersensitivity reactions initiated?

A

48-72hrs after exposure

by previously sensitized T lymphocytes

  • induces delayed type hypersensitiity rxn mediated by CD4 lymp
    (ex. tuberculin rxn, contact dermatitis)
  • induces direct cell cytotoxicity reaction mediated by CD8 lymp
    (ex. transplant rejection)
36
Q

Explain the mechanism of delayed hypersensitivity

A
  1. Initial encounter: DC + antigen–>TH-1 CD4+ cells
  2. In subsequent encounter: TH-1 cells recognize antigen presented on DC and produce cytokines

* IL-2 induced production of CD4+

*TNF & Lymphotoxins–>cause local vasodilation & increase expression of adhesion molecules that cause attachment of passing lymphocytes and monocytes. chemokines also produced, which will attract neutrophils.

37
Q

Explain T-cell mediated cytotoxicity: Hypersensitivity Type IV

A
  1. previously sensitized CD8+ cytotoxic lymphocytes attack and destroy antigen-bearing target cells
  2. They kill target cells by 2 mechanisms: Fas (CD95) induced apoptosis and by perforin-granzyme dependent killing
  3. Cytotoxic T lymphocytes produced:
    a. perforin: perforate the plasma membranes of target cells by “drilling holes” and delivery granzymes
    b. granzymes will activate capases that will induce apoptosis in target cells.
38
Q

What Hypersensitivity is this an example of?

A

Type IV: skin, delayed hypersensitivity

  • cell mediated process, not ab
  • CD4 cells in grey
39
Q

What type of transplant rejections are there?

A
  1. hyperacute
  2. Acute
  3. Chronic
40
Q

Explan hyperacute transplant rejection

A
  1. Already preformed antidonor Ab in the recipient immediately react w/ and deposit in the vascular endothelium of grafted organ
  2. Complement fixation and an inflammatory process occurs leading to destruction of the vessel wall and thrombosis of the graft vessels

minutes to hours

no treatment

prevenetion

41
Q
A
42
Q

Explain Acute Transplant Rejection

A
  1. CD4/CD8 cells encounter antigen on AP DC either w/in the grafted organ or after migration of DC to draining LN
  2. CD8 proliferate w/in the interstituim and attack the vessel walls causing endothelitis but no complete vascular wall damage occurs
  3. Similar to DS Type IV- CD4 TH-1 cells produce: IL-2, TNF, chemokines, and IFNgamma–>lymphocytic infiltration and MO activation
  4. B cells eventaully activated by helper T and the produced ab will attack the vessel walls causing vasculitis & vascular wall damage

Days to weeks

immunosuppressive agents

prevention

43
Q

What type of rejection does this picture represent?

A

Acture transplant cellular rejection

44
Q

Describe the transplant rejection in this figure?

A

acute transplant humoral rejection

-necrosis, fibrosis, kidney will be lost, a ab mediated loss.

45
Q

Chronic Transplant Rejection

A
  1. Similar to HS Type IV, Th-1 cells are activated–>cytokines:
    a. IL-2–>proliferation of T cells
    b. TNF and lymphotoxins produced will cause local vasodilation & indrease expressoin of adhesion molecules that cause attachment of passing lympho and monocytes. chemokines are produced & attract neutrophils.
    c. (Key cytokine): IFNgamma–>MO activated–>IL-1,IL2 & TNF–> inflmmation

–>MO also produce PDGF–>fibroblast proliferation cause fibrosis.

Weeks to years

No treatment

Prevention

46
Q

What type of Transplant rejection is this?

A

chronic renal transplant rejection

47
Q

Immunodeficiency Disorders

A

Congenital and acquired immunodeficiency

48
Q

X-linked Hypogammaglobulinemia (Bruton’s Agammaglobulinemia)

A
  • B cell deficiency
  • rare, low Ig and virtual absence of Mature B cells
  • Mutation on X chr- BTK gene

(plays roles in maturation of B cells)

  • recurrent infect (resp.) through childhoos. lack of B cells and low ab levels noted
  • tx: IV Ig every 3-4wks for life
49
Q

Common Variable Immunodeficiency

A
  • B cell deficiency
  • Hypogammaglobulinemia affecting all ab classes (sometimes only IgG)
  • congenital or aquired. (most congenital are sporadic, but familial cases AD or AR)
  • intrinsic B cells defect or T cell regulator defect. Circulating B cells present but cannot differentiatio to plasma cells
  • later disease onset–>recurrent infect (sinusitis, bronchitis, pneumonia)
  • high incidence of autoimmune disorders (20%) and malignancies (lymphomas, gastric carcinoma)
50
Q

Isolated IgA deficiency

A

B cell deficiency

  • relatively common, 1:600, CA
  • sporadic but familial cases AR or AD
  • maturation/diff og IgA blocked. defect in diff of IgA positive B cells into IgA producing plasma cell
  • most are asymptomatic, may have increased in diarrhea & respiratory tract infections
51
Q

Digeorge Syndrome

A
  • t cell deficiencies
  • rare syndrome, failure thymus and parathyroid development, defect in 3rd & 4th pharyngeal arches
  • deletion in chr 22 near middle chr at q11.2
  • tetany due to hypocalcemia (hypoparathryoidism), MR, Facial abnormalities, GI abnorml, Congenital heart defect
  • tx: IV Ig every 3-4 wks life
52
Q

Hyper-IgM syndrome

A

t cell deficiency

  • rare, high IgM concentrations, low IgG, IgE, IgA. normal B & T cells
  • caused by failure of IgM to switch to other abs due to mutations in the surface proteins on CD4T that interact w/ the CD40 on the surface of b cells
  • present early in life with recurrent infections
  • tx w/ pooled gamma globulins
53
Q

SCID

A

Combined B & T cell deficiency

  • B/T cells crippled or absent
  • defect in IL-2 R on T cells (most common)
  • defect adenosine deaminase (2nd most common)
  • other mutations in ZAP-70 and JAK-3
  • symptoms: recurrent infeect by bacteria, viruses, fungi, protozoa (boy in a bubble syndrome)
  • tx: bone marrow transplant, restores immunity
54
Q

Wiskott-Aldrich syndrome

A

combined B & t cell deficiency

  • rare X linked R.
  • eczema, thrombocytopenia w/ small platetelets and immunideficiency
  • mutation in short arm of Xchr known as wiskott aldrich syndrom protein
  • B/T cells affected–>abnormality is failure to mount IgM response
  • IgM (reduced), IgA & IgE (elevated), IgG (Elevated or reduced)
  • tx symptoms
55
Q

Complement deficiency

A
  • C2 deficiency most common. deficiency in classical pathway (high insidence of SLE-like illness)
  • C3 deficiency (increased pyogenic infect-Strept & staff) and increased incidence of immune-complex mediated glomerulonephritis
  • Deficiencies in C5, C6, C7, C8, C9- recurrent neisseria infect
  • C1 inhibitor deficiency-hereditary angioedema (AD)
  • decay accelerating factor & CD59 deficiency can lead to Paroxysmal noctural hemoglobinuria (PNH)

Pathology-1 (5 decks)

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