Upgrade to remove ads
Only $2.99/month

FA immunology

Terms in this set (26)

enlarged in a viral infection
T cell areas

lymph nodes -- paracortex

spleen - periarteriolar lymphoid sheath (PALS) of white pulp
germinal centers are found in
secondary follicles of lymph nodes
are ACTIVE
lymphoid drainage below the pectinate line - structures and nodes
anal canal is below pectinate line, drains into superficial inguinal nodes

other superficial inguinal node draining structures: skin below umbilicus (except popliteal), scrotum, vulva
lymphoid drainage above pectinate line - structures and nodes
lower rectum to anal canal are above pectinate line, drains into internal iliac nodes

other internal iliac draining nodes: bladder, middle 1/3 of vagina, cervix, prostate
where are B cells located in the lymph nodes and spleen
lymph nodes - follicles (primary are dense & dormant, secondary are pale & active with germinal centers)

spleen - follicles of WHITE pulp
why are patients susceptible to encapsulated bacteria post-splenectomy or with sickle cell disease
low IgM, low complement activation, low C3b opsonization
encapsulated bacteria examples
Salmonella
Streptococcus pneumoniae
Streptococcus pyogenes (GBS)
Klebsiella pneumoniae
Haemophilus influenzae (hib)
Pseudomonas aeruginosa
Neisseria meningitidis
Cryptococcus neoformans (fungi!!)

E. coli (meningeal strains)
Bordetella pertussis
Bacillus anthracis (poly D glutamate)
what vaccinates do post-splenectomy or sickle cell patients definitely need
pneumococcal (strep pneumo)
Hib
meningococcal (neisseria)
where are hassels corpuscles found? what are they?
THYMUS
contain epithelial reticular cells
hypoplastic thymus in
DiGeorge

severe combined immunodeficiency (SCID)
thymoma associated with
(a thyMUS mass)

myasthenia gravis

superior vena cava syndrome
TLRS recognize
PAMPs - pathogen associated molecular patterns

examples: TLR4 (& macrophage CD 14) recognize LPS (PAMP)

other PAMPs: flagellin of bacteria; nucleic acids of viruses
adaptive immunity variation is accomplished through
V(D)J recombination during lymphocyte development
Neutrophil chemotactic factors
bacterial products
IL-8
C5a
LTB4
genetic deficiency of FOXP3
IPEX: immune dysregulation, polyendocrinopathy, enteropathy, X-linked

also nail dystrophy, dermatitis; associated with DM in male infants
cytokines that attenuate the immune response
TGF-beta
IL-10

IL-10: decrease expression of MHC class II and ThI cytokines. Inhibit activated macrophages and dendritic cells. Also secreted by regulatory T cells.
chronic granulomatous disease - what bacteria cause recurrent infections (in particular)
catalase positive because they neutralize their own H2O2, leaving the patient's compromised phagocytes without any ROS to fight infection

Staph aureus
Pseudomonas cepacia
Serratia marcescens
Nocardia
Aspergillus (fungi)
some of the killed (inactivated) vaccines
Rabies
Influenza - injected
Polio - Salk (injected)
hepatitis A

induce mostly humoral response
some of the live attenuated vaccines
BCG
influenza - intranasal
polio - sabin (oral)
rotavirus
rubella
varicella
yellow fever
first and fast - type I hypersensitivity

Ab mediated

skin or blood test ELISA for allergen specific IgE
anaphylactic, atopic

free antigen cross links IgE on presensitized mast cells and basophils

immediate release of vasactive amines acting on POSTCAPILLARY venules - ie histamine

rapid after antigen exposure due to preformed Ab

delayed phase from mast cells and basophils releasing cytokines --> cellular inflammation
cytotoxic - type II hypersensitivity

antibody mediated

Direct Coombs for Ab attached directly to RBC surface

Indirect Coombs for unbound Ab in serum
Host Ab bind to cell surface antigens on abnormal cells, which is opsonized (coated) with Ab

destruction:
-phagocytosis and/or activation of complement
-NK cell killing (Ab dependent cellular toxicity)
(autoimmune hemolytic anemia, ITP, transfusion rxn, hemolytic dz of newborn)

inflammation:
Ab binding --> complement --> inflammation, Fc receptor mediated
(Goodpasture, RF, hyperacute transplant rejection)

dysfunction:
Ab binding --> blockade of cell fx, or activate downstream processes
(MG, Graves)
type II hypersensitivities
cell destruction:
-autoimmune hemolytic anemia
-immune thrombocytopenic purpura
-transfusion reactions
-hemolytic disease of the newborn

inflammation:
-Goodpasture syndrome (anti-GBM, lung & kidney)
-rheumatic fever
-hyperacute transplant rejection

dysfunction:
-Myasthenia gravis (anti-ACh RECEPTOR)
-Graves disease (anti-TSH-RECEPTOR)
type III hypersensitivity - immune complex

antibody mediated
IgG-Ab --> complement activation --> attract neutrophils which release lysosomal enzymes
often vasculitis, systemic effects

type III think 3 things stuck together:
Ab-Antigen-complement

-SLE
-Polyarteritis nodosa
-Poststrep glomerulonephritis
-serum sickness
-Arthus reaction
serum sickness

ab to foreign proteins, or drugs acting as haptens
complexes of Ab-antigen form, deposit in tissue, then fix complement with tissue damage

fever, urticaria, arthralgia, proteinuria, lymphadenopathy

5-10 after antigen exposure
arthus reaction

local, subacute; from intradermal injection of antigen into presensitized (has IgG) person
immune complex formation in the SKIN

edema, necrosis, activation of complement
type IV hypersensitivity

no Ab

either direct cytotoxicity via CD8+ killing

or

delayed type via CD4+ cytokines --> inflammation, macrophages
type 1 DM

contact dermatitis - poison ivy, nickel allergy

graft vs host disease

PPD and patch tests
THIS SET IS OFTEN IN FOLDERS WITH...