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1 innate and adaptive immune responses in the vaginal mucosa.
2 penetrating epithelial barriers such as the vaginal mucosa.
3 strategy for immune protection of rectal and vaginal mucosa.
4 antibodies and T cells were observed in the vaginal mucosa.
5 duced CD8(+) T-cell responses in the gut and vaginal mucosa.
6 effective delivery vehicles for siRNA to the vaginal mucosa.
7 h rate of HIV infection in women through the vaginal mucosa.
8 viral replication and spread throughout the vaginal mucosa.
9 he heterosexual transmission of HIV-1 at the vaginal mucosa.
10 ecific CD8 T cells in tissues, including the vaginal mucosa.
11 the mechanism of immune induction within the vaginal mucosa.
12 rding the phenotype of CD4(+) T cells in the vaginal mucosa.
13 to DC-SIGN(+) cells is limited in an intact vaginal mucosa.
14 defense mechanism against C. albicans at the vaginal mucosa.
15 ortant component in immune protection of the vaginal mucosa.
16 that affect immunity after challenge at the vaginal mucosa.
17 effector function from the periphery to the vaginal mucosa.
18 ent memory CD8 T cells in the intestinal and vaginal mucosa.
19 the genital tract draining nodes and in the vaginal mucosa; 2) had significantly lower virus titers;
20 common commensal of the gastrointestinal and vaginal mucosa and a leading cause of serious infections
21 er numbers of Ag-specific CD8 T cells in the vaginal mucosa and iliac lymph node, as well as 2-3x mor
22 ocal CD8(+) T cell-mediated responses in the vaginal mucosa and ILNs, the mice were protected against
23 ated responses were detected locally, in the vaginal mucosa and in the draining iliac lymph nodes (IL
24 a clade C FIV isolate via the oral-nasal or vaginal mucosa and multiple tissues were examined by vir
26 ine endometrium, endocervix, ectocervix, and vaginal mucosa) and temporally throughout the menstrual
27 at each interval consisted of vaginal wall, vaginal mucosa, and clitoris assessments; femoral vein s
28 aginal tract, and T cell responses in blood, vaginal mucosa, and draining lymph nodes that rapidly ex
29 tective Th1 immune responses to HSV-2 in the vaginal mucosa, and suggest their importance in immunity
30 viruses, transported them through explanted vaginal mucosa, and transmitted them in trans to vaginal
31 howed that 45% +/- 10% of lymphocytes in the vaginal mucosa are CD3+ compared with 75% +/- 5% in LNC
33 d in the penetration of superantigens across vaginal mucosa as a representative nonkeratinized strati
34 FIV RNA was detected in tonsil and oral or vaginal mucosa as early as 1 day p.i. by TSA-ISH and in
35 ed R5 HIV-1 entered macrophages in explanted vaginal mucosa as early as 30 min after inoculation of v
37 s via heterosexual contact, with the cervico-vaginal mucosa being the main portal of entry in women.
40 e function of Ag-specific CD8 T cells in the vaginal mucosa comparing the two routes of infection.
41 albicans infection in mice is limited at the vaginal mucosa despite a strong Candida-specific Th1-typ
42 unced diminution of virus clearance from the vaginal mucosa despite the presence of HSV-specific B an
45 decreased challenge virus replication in the vaginal mucosa, genital and neurological disease, and mo
46 nic exotoxin A, respectively, across porcine vaginal mucosa in an ex vivo model of superantigen penet
47 l receptor, which allows it to penetrate the vaginal mucosa, induce interleukin-8, and cause toxic sh
48 the mouse vagina were transported across the vaginal mucosa into draining lymph nodes, but not into d
51 to SAg profiles of skin lesion isolates and vaginal mucosa isolates revealed that the SAg profile of
52 show that the lack of APC maturation in the vaginal mucosa leads to a delay in CD8 T cell activation
53 ntigen exotoxins absorbed through the gut or vaginal mucosa, little is known regarding the pathogenes
54 ced epithelial cell membrane blebbing in the vaginal mucosa may play a role in the pathogenesis of BV
56 llenge, of antiviral effector T cells in the vaginal mucosa of female rhesus macaques immunized with
59 l persistence, showed that GBS colonized the vaginal mucosa of mice at high numbers (10(6)-10(7) CFU/
60 producible, asymptomatic colonization of the vaginal mucosa over a period of typically 3 to 4 weeks'
61 influx of lymphocytes, may cause changes in vaginal mucosa permeability, facilitating TSST-1 penetra
62 cherichia coli to carbohydrate structures of vaginal mucosa plays a major role in the pathogenesis of
63 ement of innate-mediated inflammation in the vaginal mucosa rescues this phenotype and completely inh
65 timely appearance of effector CD8 T cells in vaginal mucosa, thus further delaying viral control in t
66 thogenic and poorly transmissible across the vaginal mucosa to a variant that still maintains CCR5 us
67 he superantigen must therefore penetrate the vaginal mucosa to interact with underlying immune cells
69 of a cytomegalovirus promoter (pCMV/HGH) via vaginal mucosa (V), Peyer's patch (PP), and/or abdominal
71 he human fallopian tube, uterus, cervix, and vaginal mucosa were examined for susceptibility to infec
73 s in the systemic compartment but not in the vaginal mucosa, while the same antibodies injected intra
74 hese findings indicate that targeting of the vaginal mucosa with a Lipo/rAdv5 prime/boost vaccine eli
75 nd CD8(+) T-cell responses in the rectal and vaginal mucosa with greater functional heterogeneity tha
76 we show that these viruses replicate in the vaginal mucosa with minimal induction of antiviral inter
77 ear leukocytes (PMNs) infiltrated the murine vaginal mucosa within 24 h after intravaginal inoculatio
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