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immuno Flashcards

1
Q

PD-1 inhibitor

A

work by disrupting the binding of PD-1 on tumour cell

–> T cell programmed cell death

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2
Q

mtor inhibitors

A

prevent autonomous activity of the mtor pathway

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3
Q

ctla4 inhibitors

A

enhance ability if APCs to activate T cell

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4
Q

HIV-2

A 
– less virulent
– lower viral load
– lower rates of vertical transmission
– slower progression
– HIV-2 is less virulent.
– Seen mainly in western central Africa and southern and western India.
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5
Q

peripheral neuropathy - HAART

A

Didanosine, Stavudine and Zalcitabine

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6
Q

hypersensitivity types

A

Type 1: Specific IgE on mast cell ie: anaphylactic reaction to penicillin.
Type 2: IgG cytotoxic ie: hemolytic anemia
Type 3: Immune complex ie: serum sickness,GN
Type 4: T cell mediated ie: contact dermatitis

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7
Q

most powerful prediction from HIV to AIDS

A

CD4 count

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8
Q

strongest single predictive marker of disease progression at all stages of HIV

A

CD38 expression by CD8 cells

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9
Q

protease inhibitor s/e

- NAVIR

A
  1. lipodystrophy
    - ritoNAVIR
    - saquinavir
    - nefinavir
  2. increased risk of MI
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10
Q

HAART teratogenic

A

efavirenz

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11
Q

HIV cx

A

CD4 >200
-herpes zoster (CD 4: 200-500)

CD4 <200

  • oral candidiasis
  • HSV
  • hairy leukoplakia
  • crytosporidosis
  • toxoplasmosis
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12
Q

Heterozygosity for CCR Delta 32 in HIV

A

slower disease progression to AIDS by two fold

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13
Q

HLA-B5701

A

abacavir hypersensitivity reaction

- avoid Abacavir

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14
Q

atazanavir

A

indirect hyperbili

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15
Q

Absolute contraindication to Protease inhibitors (CYP 3A4 inhibitor)

A
  • Cisapride- torsades.
  • Lovastatin- rhabdomyolysis ** (metabolised by CYP 3A4) –> can use pravastatin
  • Midazolam-prolonged sedation
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16
Q

abacavir

A

MI (90%)

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17
Q

Immune reconstitution sydrome (IRIS)

A

symptoms include:
-high fever, increase in LN, worsened CNS lesion, worsened pulmonary infiltrate, increased pleural effusion

Rx: NSAIDS for symptom relief.
CONTINUE TB therapy and ART!!

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18
Q

hep b rx in HIV and Hepatitis B co-infection

A

For patient who require HBV treatment:
Not yet on HAART:
Truvada (Emtricitabine + tenofovir) + N-NRTI or PI

If on HAART, 2 options:
1. Lamivudine naive:
– Truvada or Lamivudine + tenofovir.
– Entecavir only if patient has full suppression of HIV

  1. On Lamivudine:
    – Add tenofovir or adefovir
    – Or change to Truvada.
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19
Q

opportunistic infection occurs at all CD4 cell counts

A

Pneumococcal pneumonia and TB

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20
Q

T helper cells

A

Th1 secrete IFN-γ, TNF, Lymphotoxin (Defence against intracellular pathogen)

Th2 secrete IL-4,IL-5,IL-6,IL-10,IL-13,TGF-β (Defence against Helminths)

Th17 secrete IL-17 (Defence against candida and staph)

21
Q

MHC

A

Class I– Intracellular proteins.Presents peptide to CD8 T cell.

Class II- extracellular proteins.Presents peptide to CD4 T cell.

22
Q

Types of T cells

A

Helper
– T- helper cells known as CD4+ T cells because they express the CD4 protein on their surface.
– Activated when presented with peptide antigen by MHC class II expressed on APC.
– Once activated, they divide and secrete cytokines
– Can differentiate into one of several subtypes, including TH1, TH2, TH3, TH17,

Cytotoxic
– Cytotoxic T cells destroy virally infected cells and tumor cells, and implicated in transplant rejection.
– Also known as CD8+ T cells
– Recognize their targets by binding to antigen associated with MHC Class I.

Memory
– Memory T cells are a subset of antigen-specific T cells that persist long-term after an infection has resolved.
– Expands to large numbers of effector T cells upon re-exposure to their cognate antigen.
– Memory T cells comprise two subtypes: central memory T cells (TCM cells) and effector memory T cells (TEM cells).
– Memory cells may be either CD4+ or CD8+.
– Memory T cells typically express the cell surface protein CD45RO.

Regulatory
– Regulatory T cells (Treg cells), formerly known as suppressor T cells, are crucial for the maintenance of immunological tolerance.
– Main role is to shut down T cell-mediated immunity toward the end of an immune reaction and to suppress auto-reactive T cells that escaped the process of negative selection in the thymus.
– Two major classes of CD4+ regulatory T cells have been described, including the naturally occurring Treg cells and the adaptive Treg cells.
– Naturally occurring Treg cells (also known as CD4+CD25+FoxP3+ Treg cells) arise in the thymus,
– Adaptive Treg cells (also known as Tr1 cells or Th3 cells) may originate during a normal immune response. Naturally occurring Treg cells can be distinguished from other T cells by the presence of an intracellular molecule called FoxP3.
– Mutations of the FOXP3 gene can prevent regulatory T cell development, causing the fatal autoimmune disease IPEX.

Natural killer
– NKT cells recognize glycolipid antigen presented by a molecule called CD1d
– Once activated, these cells can perform functions ascribed to both Th and Tc cells (i.e., cytokine production and release of cytolytic/cell killing molecules).
– They are also able to recognize and eliminate some tumor cells and cells infected with herpes viruses.

γδ
– γδ T cells (gamma delta T cells) represent a small subset of T cells that possess a distinct T cell receptor (TCR) on their surface.
– A majority of T cells have a TCR composed of two glycoprotein chains called α- and β- TCR chains. However, in γδ T cells, the TCR is made up of one γ-chain and one δ-chain.
– This group of T cells is much less common (2% of total T cells) than the αβ T cells, but are found at their highest abundance in the gut mucosa, within a population of lymphocytes known as intraepithelial lymphocytes (IELs).
– γδ T cells are not MHC restricted and seem to be able to recognize whole proteins rather than requiring peptides to be presented by MHC molecules on antigen presenting cells.

23
Q

coeliac dis

A

HLA-DQ2 or HLA-DQ8 restricted T-cell immune reaction in the lamina propria as well as an immune reaction in the intestinal epithelium

24
Q

IL 1

A
  • produced by macrophage,monocytes and dendritic cells.
  • critical for inflammatory response against infection.
  • Reset the hypothalamus thermoregulatory center causing fever.
25
Q

IL 2

A

induces proliferation of T-cells.

26
Q

IL 3

A

Hematopoietic lymphoid growth and proliferation

27
Q

IL 4

A

acts on B-cells to promote IgE switching

-Overproduction of IL-4 assoc with allergies

28
Q

IL 5

A

regulates eosinophil growth and activation

29
Q

IL 6

A

differentiation of activated B-cells to plasma cells

30
Q

IL 8

A

Neutrophil chemotaxis

31
Q

IL 11

A

stimulates megakaryocytopoiesis to produce platelets

32
Q

PAMPs assoc pathogens

A 
Bacterial:
Peptidoglycan
Bacterial DNA
Lipoteichoic acids (Gram positive)
Lipopolysaccharides (Gram negative)

RNA viruses:
dsRNA

Yeast:
Mannans.

33
Q

absence of B cells

A

X-linked agammaglobulinaemia (Bruton’s disease)

34
Q

T cell immunodeficiencies

A

1) Idiopathic CD4 lymphopenia
2) Chronic mucocutaneous candidiasis
3) Hyper-IgE syndrome

35
Q

X linked SCID

A

Deficiency of cytokine receptor γ common chain

Autosomal recessive SCID:
Jak 3 deficiency
IL-7Rα deficiency
ZAP 70 defieiency
CD3 deficiency
RAG-1,2 deficiency
Myeloid or reticular dysgenesis.
36
Q

Disorders of neutrophil phagocytic function

A

1) Chronic granulomatous disease
2) Leukocyte adhesion deficiency
3) Chediak-Higashi Syndrome
4) Neutrophil enzyme deficiency-G6PD,MPO

37
Q

NOD-like receptor group responsible for the acute inflammation seen in gout

A

NALP 3

-Monosodium urate crystals(MSU) and Calcium pyrophosphate dihydrate(CPPD) activates the NALP3 inflammasome

38
Q

Dendritic cells function

A

– superb APC

– Lurks in tissues as sentinels.
– Activates quiescent naive and memory T(Th,Tc) and B cells.
– Highly potent activators even with low levels of antigen.
– Two distict types: conventional(cDCs) and plasmacytoid(pDC)

Plasmacytoid DC expresses TLR7(RNA virus) and TLR9(DNA virus) in endosomes and induces rapid anti-viral state.

39
Q

Hereditary Angioedema

A

-deficiency of C1 inhibitor leading to continuous activation and consumption of C4 and C2.
– C2 is responsible for kinin release that results in vasodilation and increased vascular permeability leading to angioedema.

Clinical presentation:
– Typically school age.
– Recurrent edema that is non pruritic, painless, non whealing and usually resolves within 72 hours.
– Edema can be cutaneous,laryngeal and abdominal (mimics acute abdomen-early diagnosis may avoid unnecessary surgery!!)

Treatment:

  • C1-inhibitor concentrate.
  • Danazol if frequent attacks
  • Tranexamic acid
  • ε-aminocaproic acid
40
Q

APC

A

External antigen: dendritic cell, macrophage, B-cell (express MHC II)

Internal antigen: All MHC class I positive cells (express MHC I)

41
Q

serum beta 2 microglobulin

A 
component of the HLA class I molecule
-Clinically relevant in reflecting cell turnover

Prognosis in Multiple myeloma and HIV.
-The higher the worse.

42
Q

Serum tryptase

A

Tyrptase helpful if collected within 3 hours of IgE mediated reaction.

Used to distinguish mast cell dependent anaphylaxis from other systemic event.

Does NOT differentiate between IgE and non-IgE mediated causes.

43
Q

most specific for the diagnosis of NSAIDs hypersensitivity

A

Basophil activation test

44
Q

acute phase reaction

A

-IL-1, IL-6 and IL-8, and TNF-α

Positive acute phase proteins (Increase in inflammation):

  • C-reactive protein,
  • Mannose-binding protein,
  • complement factors,
  • ferritin,
  • ceruloplasmin,
  • Serum amyloid A and
  • haptoglobin.
  • serpins.
  • Alpha 2-macroglobulin

Negative acute phase protein (decrease in inflammation): mnemonic “ATTTRA”.

  • albumin,
  • transferrin
  • transthyretin
  • transcortin
  • retinol-binding protein
  • antithrombin
45
Q

IgG4-positive multiorgan lymphoproliferative syndrome

A

Characteristic features of IgG(4)+MOLPS are as follow:

1) Serum IgG4 is prominently elevated,
2) IgG4-positive plasma cells infiltrate in involved tissues
3) various mass-forming lesions with fibrosis develop in a timely and spatial manner
4) good response to corticosteroids.
5) no positivity of anti-SS-A/SS-B antibodies

Organ system affected by IgG(4)+MOLPS:

1) autoimmune pancreatitis
2) lacrimal and salivary gland (Mikulicz’s disease)
3) retroperitoneal fibrosis
4) IgG4-associated nephropathy

46
Q

CTLA 4

A

generates a NEGATIVE signal
-Stimulating CTLA4 –> Block the immune response
Anti-CTLA4 stimulates the immune response by blocking CTLA4

47
Q

hereditary angioedema mx

A

Acute management includes:

1) C1-INH concentrate from donor blood
2) FFP if in emergency as FFP contains C1-INH.
3) Kallikrein inhibitor (Ecallantide)- inhibits plasma kallikrein.
4) Bradykinin inhibitor (Icatibant)- inhibits bradykinin B2 receptor.

Prophylaxis:

1) Danazol- Androgens increase production of C1-INH in the liver.
2) Tranexamic acid- fibrinolysis inhibitors

The condition does NOT respond to antihistamines, corticosteroids, or epinephrine.

48
Q

HLA

A

HLA Class I:
- HLA- A, B, C (E,F,G,H)

HLA Class II:
- HLA- DR, DP, DQ(DM and DO)

HLA-DR alpha chain is invariant (unchanged) while HLA-DR beta chain is very polymorphic.

Some disease associations:
Ankylosing spondylitis HLA B27
Rheumatoid arthritis HLA DR4
Autoimmune conditions (SLE, Addisons, Type 1DM, Grave’s, Myasthenia) HLA DR3.

Transplant and HLA:
– Acute graft rejection caused by cross reactivity of T cell receptors for foreign MHC.

49
Q

Types of hypersensitivity

A

Type I – Anaphylactic

  • antigen reacts with IgE bound to mast cells
  • anaphylaxis, atopy

Type II – Cell bound

  • IgG or IgM binds to antigen on cell surface
  • autoimmune haemolytic anaemia, ITP, Goodpasture’s

Type III – Immune complex

  • free antigen and antibody (IgG, IgA) combine
  • serum sickness, systemic lupus erythematosus, post-streptococcal glomerulonephritis, extrinsic allergic alveolitis (especially acute phase)

Type IV – Delayed hypersensitivity

  • T cell mediated
  • tuberculosis, tuberculin skin reaction, graft versus host disease, allergic contact dermatitis, scabies, extrinsic allergic alveolitis (especially chronic phase)

In recent times a further category has been added:

Type V – Stimulated hypersensitivity

  • IgG antibodies stimulate cells they are directed against
  • Graves’, myasthenia gravis

bpt (18 decks)

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