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Immunology > Immunodeficiencies > Flashcards

Immunodeficiencies Flashcards

1
Q

Lab tests for T-cell

A

Flow cytometry, functional assays (mitogen response, MLR, DTH skin test)

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2
Q

B-cell lab tests

A

circulating antibodies, flow cytometry

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3
Q

Macrophage lab test

A

Enumeration (=flow cytometry), nitroblue tetrazolium for function

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4
Q

Complement lab test

A

direct measurement of complement components, hemolysis assay

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5
Q

What does each system specialize in? What happens if it’s impaired?

  1. B-cells
  2. T-cells
  3. Phagocytes
  4. Complement

Which deficiecnies would cause cancer?

A
  1. B-cells (humoral, adaptive)= pyogenic bacteria= staph, strep, hemoph. Respiratory, GI, skin infections, sepsis, meningitis
  2. T-cells (cell mediated, adaptive)= Intracellular organisms= viruses and then bacteria. Viral infections. Increased risk of cancer when immunodeficient
  3. Phagocytes- catalase postive bacteria (Staph, kleb, e.coli); fungi lymphadenitis, skin liver, lung abcesses
  4. Complement- pyogenic bacteria, viruses systemic bacterial infections
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6
Q

X-linked agammaglobulinemia

  1. symptoms
  2. defect
  3. therapy
A

B-cell deficiency

  1. recurrent bacterial infections
  2. no BTK= b-cells arrested at pro-Bcell stage
    3.
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7
Q

C3 Def

A

Recurrent infection with G- bacteria

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8
Q

Factor I def

A

low C3= susceptibility to encapsulated bacteria

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9
Q

C5-C9 def

A

No MAC complex, increased Neisseria infections

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10
Q

NEMO deficiency

A

No NFkB activation= no T-cell activation

Chronic bacterial and viral infections, developmental defectc

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11
Q

MBL def

A

No lectin pathway, less phagocytosis.

Infections from n. meningitidis

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12
Q

Chronic Granulomatous disease

A

NOX1 gene, no NADPH oxidase= impaired neutrophil function.

No respiratory burst= no phagycytes to kill bacteria.

Chronic bacterial and viral infections.

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13
Q

NK cell def

A

GATA2 gene, HSV infections

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14
Q

Hyper IgM

A

Defect in AICDA (activation induced cytosine deaminase), CD40, CD40L, IKBKG.

No isotype switching or somatic hypermutation

ECF bacterial and fungal infections

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15
Q

IgG2 def

A

encapsulated bacteria

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16
Q

SCID

A

No B-cell and T-cell function

Caused by: ADA, PNP def, thymic aplasia

All infections

**X-linked SCid gammac chain= T-cells only, bubble boy**

17
Q

Omenn Syndrome

A

Rag1/Rag2 gene= impaired VDJ recombination.

All infections

18
Q

MHC I def

A

TAP1/TAP2 = no MHC I receptors

Respiratory viral infections

19
Q

Pre-B cell receptor def

A

No B-cells/antibodies

Persistnet bacterial infections

20
Q

DiGeorge

A

no thymus and t-cells= all infections

21
Q

APECED

A

AIRE defect, less T-cell tolerance for self-antigens

Autoimmune

22
Q

IPEX

A

FoxP3 gene; lack of Treg cells and peripheral tolerance. Autoimmune

23
Q

ZAP70 defect

A

T-cells cannot signoalr through antigen receptors

all infections

24
Q

C4a, C4b

A

Reduced clearance of immune complexes

autoimmune disease and infections

25
Q

Selective IgA def

A

MOST COMMON!!

No IgA= respiratory infections

26
Q

Wiskott-Aldrich Syndrome

A

X-linked, defective WASP gene= Defective anti-polysaccharide Ab and impaired T-cell activation

Susceptible to encapsulated ECF bacteria

27
Q

Leukocyte Adhesion deficiency

A

Phagocytic cell defect

CR3, CR4 and LFA-1 adhesion defects= defective migration of monocytes and neutrophils==>widespread infection from encapsulated bacteria.

28
Q

Chedlak-Higashl SYndrome

A

Phagocyte problem

  • Lysosomal traffiking regulator protein defect
  • Defective fusion of endosome and lysosome, defective phagocytosis
  • Recurrent/persistent bacterial infections, granuloma formation
29
Q

Causes of secondary immunodeficiencyes

A
  • Steroids, cytotoxic drugs, chemotherapy, irradiation
  • AIDs (no CD4 cells)
  • Nutritionals (protein, calorie, biotin, B12, iron)
  • Post infections
  • Cancer metastases to bone marrow
  • Asplenia
30
Q

HIV–> AIDs

  • when is it AIDs
  • How does the HIV infection happen (receptors?)
  • What does HIV NEED for replication?
A

<500CD4 cells

HIV gp120 binds CCR5 or CXCR4= endocytosis

  • CCR5=M-tropic-Virus infects macrophages, CD and some t-cells= spread of virus to others
  • CXCR4=t-tropic- virus infects T-cells= disease

HIV replication requires T-cell activations= NFKB

31
Q

How is HIV so effective?

A
  • changes viral antigens and enzumes
  • targes CD4 TTcells
  • HIV evades host immune systm (via error prone reverse transcriptase)
32
Q

Antigenic drift

A

Mutation of serotypes/antigens on outside= epidemic

Pandemic=

33
Q

HSV strategies (x2, CMV does one of them too)

A
  1. reduce IFN-g effect on MHC I= no recognition of APC by CD4 **CMV does this too
  2. Inhibition of TAP= no peptide presentation via MHC I
34
Q

How do viruses evade humoral immunity?

A

Virally encoded complement control prtoein= less complement activation. ==Vaccinia does this.

35
Q

How do viruses inhibit inflammatory response?

A
  • Produce soluble cytokine receptors–cytokines bind viral receptors instead of host= no inflammation (wastes cytokines)= vaccinia
  • Encoding IL-10 (EBV)
36
Q

How doe these pathogens subvert the immune system?

  1. M. Tb
  2. Listeria
  3. terponema pallidum
  4. Staph
  5. Mycobacteria
A
  1. M. Tb= prevent phago=lysosome fusion
  2. Listeria= escapes phagosome
  3. terponema pallidum= coats itself with human protiens
  4. Staph= makes super antigen- polyclonal t-cell activation (no specificity)- binds CD28 and TCR of t-cell, and MHCII of APC
  5. Mycobacteria= induces Th2 response
37
Q

During pregnancy, immune response is?

Autoimmune diseases improve/worsen?

A

Reduced- don’t want to reject fetus

  • FActors: a-fetoprotein, IL10, TGF-beta
  • improved autoimmune disease states until birht, then rebounds
  • Lupus gets worse.

Immunology (12 decks)

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