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Flashcards in Immunology Deck (81)
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1

Lymph node

Follicle= B-cells
- Primary: dense, dormant
- Secondary: pale, active

Medulla=
- Cords: lymphocytes and plasma cells
- Sinuses: reticular cells and macrophages; communicate with efferent lymphatics

Paracortex= T cells (between follicles and medulla)
- Endothelial venules: B-cell entry from blood
** Underdeveloped in DiGeorge syndrome

2

Lymph drainage

Rectum (above pectinate line): internal iliac

Anal canal (below pectinate line): superficial inguinal

Right lymphatic duct: drains right arm, right chest, right 1/2 of face
- Thoracic duct drains everything else

3

Sinusoids of spleen

Vascular channels in red pulp
- Fenestrated; macrophages nearby

White Pulp:
- T cells= periarterial lymphatic sheath (PALS)
- B cells= follicles

Macrophages remove encapsulated bacteria (IgM--> complement--> C3b opsonization--> macrophage removal)
- Strep pnumo, H. flu, N. meningitidis, Salmonella, Klebsiella, Strep agalactaciae (group B)

Post-splenectomy:
- Howell-Jolly Bodies (nuclear remnants in RBCs)
- Target cells (excess membrane: hemeglobin ratio)
- Thrombocytosis

4

Thymus

Epithelium of 3rd branchial pouches

Cortex= dense, immature T cells
- Positive selection (MHC class restriction: T cells expressing TCRs binding self MHC)

Medulla= pale, mature T cells, Hassall's corpuscles
- Negative selection (non-reactive to self antigens: high affinity for self--> apoptosis)

5

Innate immunity

Neutrophils, macrophages, dendritic cells, NK cells, complement

6

Adaptive immunity

Recognize pathogen--> V(D)J recombination
- Slow response at first, memory faster
- T cells, B cells, circulating antibody

7

MHC I

HLA-A, B, C

1. Nucleated cell (any) infected with antigen
2. Processed in RER (+ intracell peptides)
3. Presented on MHC-I + Beta-2 microglob
4. Binds TCR, CD8 T-cells

** Mediates viral immunity

8

MHC II

HLA-DR, HLA-DP, HLA-DQ

1. Antigen presenting cell infected
2. Antigen processed in acidic endosome
3. Presented on MHC-II (peptide binding groove)
4. Binds TCR, CD4 T-cells

9

HLA-A3

Hemochromatosis

10

HLA-B27

Psoriasis
Ankylosing Spondylitis
Inflammatory bowel disease
Reiter's syndrome

11

HLA-DQ2/DQ8

Celiac disease

12

HLA-DR2

Multiple sclerosis
Hay fever
Systemic Lupus Erythematosis
Goodpasture's disease

13

HLA-DR3

Diabetes Mellitus, Type 1
Grave's disease

14

HLA-DR5

Pernicious anemia--> B12 deficiency
Hashimoto's thyroiditis

15

Natural killer cells

Induce apoptosis of virally infected + tumor cells
- Only lymphocyte in innate immune system

Enhanced by IL-2, IL-12, IFN-beta, IFN-alpha

Kills target cell with:
- Nonspecific activation signal
- Absence of class I MHC

16

B-cell produced antibody functions

Type I hypersensitvity reaction: IgE produced (Allergy)

Type II reaction: IgG, IgM (Cytotoxic)

Type III reaction: IgG (immune complex)

** Hyperacute, humorally mediated acute/chronic organ rejection

17

T-cell functions

Type IV delayed cell-mediated hypersensitivity

CD4+ T cells= help B cell antibody production, make cytokines
- IL-12--> Th1 cell
- IL-4--> Th2 cell

CD8+ T-cells= Cytotoxic t-cells: kill VIRUS infected cells, neoplastic, donor graft cells. Secretes granules that contain:
- perforin (deliver granules into target cell)
- granzyme (serine protease= activates apoptosis in target cell)
- Granulysin (antimicrobial, induces apoptosis)

Regulatory T-cell (Treg)
- Express CD3, CD4, CD25 (alpha chain of IL-2 receptor)
- Activated--> anti-inflammatory IL-10, TGF-beta

18

Dendrite cell

ONLY APC that can activate naive T-cell
1. Phagocytoses foreign body
2. Presented on MHC II--> Th (CD4+ cell) OR Presented on MHC I--> Cytotoxic (CD8+)
3. Costimulation: B7 on dendrite--> CD28 on Naive T-cell

19

B cell activation/class switching

Th1 or Th2 (helper CD4+ T-cell) activated
1. B-cell endocytosis foreign antigen
2. Antigen presented on MHC II--> recognized by TCR on Th cell
3. CD 40 on B-cell binds CD40Ligand on Th cell
4. Th cell secretes cytokines--> Ig class switching of B cell
5. B cell matures, produces antibodies

** Mature B cells= IgM and IgD on surface
- Differentiate into plasma cells secreting IgA, IgE, IgG

B-cell receptors:
- Ig (duh)
- CD19, CD20, CD21 (EBV receptor), CD40, MHC II, B7

20

Th1 cell

Helper T-cell
1. Secretes IFN-gamma
2. Activates macrophages
3. Inhibited by IL-4, IL-10 (from Th2 cell)

21

Th2 cell

Helper T-cell
1. Secretes IL-4, IL-5, IL-10, IL-13
2. Recruits eosinophils for **Parasite defense**, promotes B-cell production of IgE
3. Inihibited by IFN-gamma (from Th1 cell)

22

Antibody structure

Fab= Antigen binding fragment
- Only 1 antigenic specificity per B cell

Fc=
- Constant
- Carboxy terminal
- Complement binding at CH2
- Carbohydrate side chains
- (Macrophage binds at CH3)

Diversity: Random, or somatic hypermutation after antigen stimulation

Role of Abs:
- Opsonization
- Neutralization: prevent bacterial adherence
- Complement activation: enhanced opsonization

23

IgG

Secondary response (delayed)
Most abundant

Roles:
- Fixes complement
- Crosses placenta
- Opsonizes bacteria
- Neutralizes toxins, viruses

24

IgA

Prevents bacterial/viral attachment to mucous membranes

Roles:
- Does NOT fix complement
- Does NOT cross placenta
- Circulation= monomer
- Secretion= dimer; crosses epithelial cells via trancystosis, picks up secretory component in epithelial cells

25

IgM

Primary response (immediate)

Roles:
- Fixes complement
- Does NOT cross placenta
- Monomer (on B cell) or Pentamer

26

IgE

Type I hypersensitivity reaction

Roles:
- Binds Mast cells/basophils
- Cross-links when exposed to allergen
- Releases histamine from mast cells
- Activates eosinophil reaction to worms

27

Antigen type and memory (thymus dependent vs independent)

Independent: antigen LACKS peptide component
- Cannot be presented by MHC (no peptide to present to T-cells)
- Ex: LPS from gram-neg bacteria, polysaccharide capsule
- NO immunologic memory

Dependent:
- Antigens contain protein component
- Ex: Diphtheria toxoid vaccine
- Class switching and memory due to B-cell Th cell CD40-CD40L interaction

28

Complement pathway

Leads to formation of MAC (membrane attack complex) to defend against gram NEGATIVE bateria

Activation:
1. Classic= IgG/IgM mediated
2. Alternative= microbe surface molecules (attract C3b)
3. Lectin= mannose/sugars on microbe

C3b= opsonization, clears immune complexes
C3a, C5a= anaphylaxis
C5a= neutrophil chemotaxis
C5b-C9= MAC formation--> cytolysis

** Pathway inhibited (from attacking self) by Decay-accelerating factor (DAF) and C1 esterase inhibitor

29

C1 esterase inhibitor deficiency

Hereditary angioedema
- ACE-I contraindicated

30

C3 deficiency

Recurrent pyogenic sinus, resp tract infections
- Increased susceptibility to Type-III hypersensitvity reactions (immune complex)