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1 microvasculature in a two-challenge model of contact sensitivity.
2  Abs can recruit effector T cells to mediate contact sensitivity.
3 ese populations in models of anaphylaxis and contact sensitivity.
4 a relevant population of T cells involved in contact sensitivity.
5 ress has no effect on the course of irritant contact sensitivity, an immune reaction that does not in
6 ter of dermatitis patient's patch tested for contact sensitivity and (ii) the Danish National Patient
7 fect of C5L2 deficiency in a murine model of contact sensitivity, and second to determine whether the
8                            Thus, in allergic contact sensitivity, as in isolated human neutrophils, C
9 nt soluble T cell receptors (sTCR) protected contact sensitivity (CS) effector T cells from down-regu
10 ectrum antibiotic enrofloxacin will modulate contact sensitivity (CS) in mice.
11 xperiments examined a two-challenge model of contact sensitivity (CS) in which Treg abundance in the
12       T-cell tolerance of allergic cutaneous contact sensitivity (CS) induced in mice by high doses o
13                                              Contact sensitivity (CS) is related to delayed-type hype
14                 T cell recruitment to elicit contact sensitivity (CS) requires a CS-initiating proces
15                           The elicitation of contact sensitivity (CS) to local skin challenge with th
16                               Elicitation of contact sensitivity (CS), a classic example of T cell-me
17 yed-type hypersensitivity responses, such as contact sensitivity (CS), in mast cell-deficient mice wh
18 tive transfer of immune cells lacking CD3(+) contact sensitivity effector T cells, or after transfer
19 ammation in Th2-driven asthma and Th1-driven contact sensitivity experiments.
20           Moreover, FTS-A inhibited Rap1 and contact sensitivity far better than FTS.
21                       We observed diminished contact sensitivity in mice lacking FcepsilonRI or mast
22  may serve as a possible therapeutic tool in contact sensitivity in particular and T-cell-mediated in
23             Thus, anti-T11(1) mAb suppressed contact sensitivity in vivo in the transgenic/knockout m
24                                 Induction of contact sensitivity increased the proportion of motile T
25  large and long lasting increase in allergic contact sensitivity or delayed-type hypersensitivity, an
26 esponsiveness was hapten specific, since the contact sensitivity reaction of mAb-treated mice to oxaz
27                         Extensive studies of contact sensitivity reactions in mice established a mech
28 pathological (e.g., autoimmune reactions and contact sensitivity reactions such as that to poison ivy
29 ems totally reversed the failure to induce a contact sensitivity response to dinitrofluorobenzene (DN
30     However, the ability to induce a primary contact sensitivity response was completely restored in
31                                          The contact sensitivity response was significantly reduced (
32                                              Contact sensitivity responses require both effective imm
33  hairless cub/cub mcub/mcub mice show normal contact sensitivity responses to oxazolone.
34  the regulation of cognate immunity, such as contact sensitivity responses.
35 ment in non-UV-irradiated mice did not block contact sensitivity responses.
36 pic dermatitis are likely to have suppressed contact sensitivity secondary to their disease whereas s
37 P-10 and KC expression during elicitation of contact sensitivity, suggesting CD4+ T cells inhibit the
38                         Immune regulation of contact sensitivity to the poison ivy/oak catechol was s
39                                              Contact sensitivity was markedly impaired in IgE(-/-) mi