Unit 10 - 5 Immunology

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WIndow of vulnurability

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During a normal menstrual cycle, there is a period lasting 7–10 days when important components of innate, humoral, and cell-mediated immunity are suppressed by estradiol and/or progesterone, enhancing the potential for viral infection (HIV). Onset of the “window of vulnerability” coincides with an increase in estradiol at about the time of ovulation.

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effects of estrogen and progesterone on inflammation

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In general*, estrogen augments inflammatory immune responses
In general*, progesterone suppresses inflammatory immune responses

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effect of pregnancy on autoimmune dz

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Pregnancy is an immunosuppressed state* (possibly because levels of progesterone and cortisol are high)
Symptoms of some autoimmune diseases (thyroiditis, multiple sclerosis) tend to lessen during pregnancy
Autoimmune diseases tend to flare up post-partum (possibly because hormonal effects of prolactin and estrogen predominate)

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one dz exception to pregnancy being an immunosuppressed state

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SLE flareups tend to occur during pregnancy

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MS and pregnancy

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T cells (Tregs) and responsible for many of Treg suppressive effects. Expansion of Tregs together with hormonal changes (progesterone)

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extravillous trophoblasts

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source for soluble HLA-G -> facilitates Treg generation and induction

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antiphospholipid syndrome manifestations

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recurrent thromboses (venous and arterial), repeated miscarriages, cardiac valve vegetations

ass w/ lupus

can cause placental thrombus or defective placentation by inhibiting proliferation of trophoblasts

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describe the antigenic epitopes bound by antiphospholipid antibodies (aPLs)

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aPLs directed against epitopes of proteins only revealed whent hey complex w phospholipids (B2GPI - plasma protein that exists in two conformations - open and circular

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MOA for aPL induced thrombosis

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Endothelial cell damage (aPLs induce a procoagulant and proinflammatory endothelial phenotype)
Monocyte activation (aPLs induce tissue factor expression and production of cytokines)
Platelet activation (aPLs binding potentiates platelet aggregation)
Inhibition of anticoagulant activity (aPLs interfere with the components of the coagulation cascade)

a second hit of complement activation necessary for clot formation in vivo

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tests for APS

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ELISA for anti-B2GPI, or anti cardiolipin (aCL), clotting assays for lupus anticoagulant (extend clotting time in vitro, in vivo they are prothrombotic)

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ass of APLs with anticardiolipin and false positive test for syphilis

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Cardiolipin = phospholipid compnent of mito membrane (organ w lots of mito = high expression, ie heart); cardiolipin from bovine heart used ins erologic testing for syphillis (RPR); pts infected w Treponema also develop anti-cardiolipin antibodies

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tests administered to Rh negative pregnant women

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Rh-negative pregnant women receive “antibody screen” (aka indirect Coombs test) to determine if they developed anti-RBC antibodies in the serum*
If the test is positive, “antibody identification test” is performed to identify the specific antigen (e.g. Rh factor)**
If the mother does not already have anti-Rh antibodies, she can be treated with RhoGAM to prevent the development of anti-Rh antibodies (sensitization)

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Rho(D) immuneglobin

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RhoGAM; IgG anti-Rh ab given to motheres to sensitize them to Rh antigen (prevents mother from producing anti-Rh antibodies in response to RBCs from her baby)

never administer live vaccines during pregnancy

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four major types of Cd4+ effector T cells

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Th1 (proinflammatory), secrete IFN-gamma
TH17 cells (influenced b TGF-B and IL-6, IL-17 recruits leukocytes)
TH2 cells (antiinflammatory); secrete IL10,4,13, promote alternative macrophage activation (macrophages secrete tGF-beta = antiinflammatory)
Tregs (CD25+) anti inflammatory, secrete IL-2 and TGF-Beta, promote alternatve mac activation too

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pregnancy loss due to infection

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Infection may lead to fetal demise as a result of severe systemic maternal illness (eg. Influenza), pacental dysfunction due to placental infection ( eg. Malaria), or fetal systemic illness ( eg, Escherichia coli).

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mycoplasma homminis vs ureaplasma

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M. hominis metabolizes arginine but not glucose.
Ureaplasma hydrolyzes urea .

both have fried egg appearance

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synergism btwn encapsulated anerobes (prevotella) and aerobes (s. pyogenes)

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Prevotella bivia (once called Bacteroides bivia) is very frequently associated with Intraamniotic infection.
Prevotella are encapsulated Gram negative rods which are very small

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fusobacterium and pregnancy

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Gram negative, anaerobes; Long filamentous fusiform bacilli
Strongly associated with Chorioamnionitis and appears to play a role in spontaneous preterm births.

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trichomonas and pregnancy

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There is a strong association (30% greater likelihood) with premature rupture of the fetal membranes, preterm birth, low birth weight.

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listeria in pregnancy loss

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It is characterized by granulomatosis infantisepticum that may result from transplacental transmission.
Disseminated abscesses and/or granulomas in multiple internal organs of the infant

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listeria cell to cell spread

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actin rocket

Listeria thus goes from gut epithelial cells (enterocytes) to macrophages, which disseminate the bacteria throughout the body, and then it can be transferred from macrophages to endothelial cells that line the microvasculature in the meningeal membranes. In this way the meninges and the CSF are colonized.

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Parvo B19 infection during pregnancy

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Erythroid precursor cells;
Receptor: Erythrocyte P antigen -> anemia/aplastic anemia

can lead to fetal hydrops

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candida albicans

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intrauterine candidal infections are rare; unique bc it can infect without rupture of the fetal membranes


Severe funisitis ( inflammation of the umbilical cord) and acute chorioamnionitis without villitis are the hallmarks of candidal infection . The classic finding is multiple small green and or white abscesses on the surface of the umbilical cord. The presence of invasive hyphae in the cord is a risk factor for hematogenous dissemination to the fetus in whom infection is rare and often catastrophic.