IMM2022 Study Guide - Final Guide: Adaptive Immune System, Prostaglandin E2, Peptostreptococcus
Reproduction and the immune system
MHC influences body odour attracted to
opposite MHC in a partner
INNATE IMM IN THE FRT
Physical barriers include the keratin layer on
vulva which prevents adhesion and the mucus
layer in the vaginal wall the traps microbes.
There is a low PH (created by the commensal
bacteria eg lactobacillus), phagocytic cells,
TLRs (can produce a type I IFN response which
stops viral replication at a transcriptional or
translational level. NFkB response. Vaginal
epithelium have TLRs and secret
antimicrobials, cytokines, SLP1 (secretory
leukocyte protease inhibitor).
Vaginal commensals include
peptostreptococcus, lactobaccilus,
clostridium. These produce antimicrobial
produces such as lysozymes and cytokines.
The major anti-microbials after TLR
stimulation are
• Alpha-defensins (human neutrophil
peptides)
• Beta-defensins
• Calprotectin (neutrophils mucus)
• Lysosome
• Lactoferrin (antimicrobial)
UPPER FRT
• Single cuboidal epi
• Lots of neutrophils, DC, macrophage,
CD4, CD8 and langerhans cells
• Note that adaptive cells are not
usually present when healthy
LOWER FRT
• Stratified squamous
• NKC
• Lactic acid
• Ph4
• Commensals
Adaptive imm consists of CD4 and CD8 in
regional LN found in sub epithelial LP and
mucosal epithelium. IL-17, Il-23 and B-
defensin 2 are released in response to candida
albicans. B cells are activated in region LN
in endocervix. IgG is vagina from circulation.
IgA in response to pathogens, dimer form.
SEX AND THE IMMUNE SYSTEM
Females DO NOT have central tolerance to
sperm and are capable of mounting and IMM
response. Semen in the vagina influx of
neutrophils and macrophages. There can be T
cells but most women do not induce an
adaptive immune response.
SEMEN HAS IMMUNOSUPPRESSIVE
QUALITIES
Prostaglandin E2
• Inhibits IL-2 and blocks CD4 activation
• Inhibits IFNy blocking macrophage
activation
• IL-10 production
TGF-B (immune calming cytokine) which leads
to tolerance. Women who have frequent sex
have increased IgG and decreased IgA.
(decreased IgA is due to evolutionary pressure
and increased IgG is due to increased
likelihood of infection.
Note that due to the immunosuppression that
semen causes females have a decreased
ability to response to pathogens that may be
present in the male ejaculate.
IMMUNE EVASION OF SPERM
Sperm express HLA-G interacts with
immune cells
• APC target induction of tolerogenic
APC
• TC target inhibit proliferation, CTL
lysing, IFNy secretion. Induce Th2 and
Tregs.
• NKC target inhibit proliferation,
lysis through HLA-E
Document Summary
Mhc influences body odour attracted to opposite mhc in a partner. Physical barriers include the keratin layer on vulva which prevents adhesion and the mucus layer in the vaginal wall the traps microbes. There is a low ph (created by the commensal bacteria eg lactobacillus), phagocytic cells, Tlrs (can produce a type i ifn response which stops viral replication at a transcriptional or translational level. Vaginal epithelium have tlrs and secret antimicrobials, cytokines, slp1 (secretory leukocyte protease inhibitor). Adaptive imm consists of cd4 and cd8 in regional ln found in sub epithelial lp and mucosal epithelium. Il-17, il-23 and b- defensin 2 are released in response to candida albicans. B cells are activated in region ln in endocervix. Females do not have central tolerance to sperm and are capable of mounting and imm response. Semen in the vagina influx of neutrophils and macrophages. There can be t cells but most women do not induce an adaptive immune response.