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1  stimulated with OVA (assay for induction of delayed hypersensitivity).
2 ir recipients failed to display RPE-specific delayed hypersensitivity.
3 owed the capacity to suppress donor-specific delayed hypersensitivity.
4 roinflammatory Th1 cells in a mouse model of delayed hypersensitivity.
5 nship including onset patterns suggestive of delayed hypersensitivity, alongside consistent HSV featu
6 red the HLA loci in 98 Spanish patients with delayed hypersensitivity and 315 with immediate hypersen
7 with spleen cells that suppress RPE-specific delayed hypersensitivity and autoimmune rejection.
8                      The absence of systemic delayed hypersensitivity and complement-fixing Abs in th
9 ere tested for suppression of DBA/2-specific delayed hypersensitivity and concomitant immunity.
10 . into naive recipients induced allospecific delayed hypersensitivity and elicited delayed hypersensi
11 e recipients were evaluated for RPE-specific delayed hypersensitivity and examined clinically and his
12 a2 induce immune deviation in vivo (impaired delayed hypersensitivity and IgG2a Ab production) when i
13 these types of grafts display donor-specific delayed hypersensitivity and in vitro proliferating prim
14 1 is functionally relevant in the genesis of delayed hypersensitivity and may be a useful therapeutic
15 f IFN-gamma, induce macrophage cytotoxicity, delayed hypersensitivity, and enhanced cellular immunity
16                     Th1 cells, which mediate delayed hypersensitivity, are the polar opposites of CD4
17                Ag-specific proliferation and delayed hypersensitivity, as well as mitogen-induced IFN
18 geneic mice elicited an intense RPE-specific delayed hypersensitivity associated with a vehement cell
19 binding proteins inhibit local expression of delayed hypersensitivity by a T-cell fibronectin-depende
20 stered therapeutically to animals undergoing delayed hypersensitivity can almost completely abolish T
21 genotyped the MHC region in 24 patients with delayed hypersensitivity compared with 20 patients with
22  fragments were evaluated for donor-specific delayed hypersensitivity (DH) and ACAID, and fragment-co
23 recipients were evaluated for acquisition of delayed hypersensitivity (DH) and cytotoxic T cells (Tc)
24 opulations of regulatory T cells that impair delayed hypersensitivity (DH) by two different mechanism
25 lenic CD8+ effector cells which downregulate delayed hypersensitivity (DH) in immunized mice.
26                Acquisition of donor-specific delayed hypersensitivity (DH) was also assessed in recip
27 ologically and acquisition of donor-specific delayed hypersensitivity (DH) was assessed at selected i
28                     Ovalbumin (OVA)-specific delayed hypersensitivity (DH) was not impaired when OVA
29 nduces an Ag-specific impairment of systemic delayed hypersensitivity (DH), termed anterior chamber a
30 n (ACAID), is characterized by impairment of delayed hypersensitivity (DH).
31 urans can result in either immediate (IH) or delayed hypersensitivity (DH).
32 sitize recipient mice to donor alloantigens (delayed hypersensitivity, DH) was evaluated.
33 ecific delayed hypersensitivity and elicited delayed hypersensitivity directed at alloantigens.
34 (a) of T-cell activation in vitro and (b) of delayed hypersensitivity expression in vivo.
35  ear pinnae of normal BALB/c mice (assay for delayed hypersensitivity expression) or coinjected with
36 lar immune privilege, prevents Th1-dependent delayed hypersensitivity from developing in response to
37 ure TGFbeta and suppressed the expression of delayed hypersensitivity in a local adoptive transfer as
38 ed regulatory lymphoid cells that suppressed delayed hypersensitivity in naive recipients.
39 ulatory T cells that suppressed RPE-specific delayed hypersensitivity in naive syngeneic recipients.
40 ls in vitro and suppressed the expression of delayed hypersensitivity in vivo.
41 ess the induction and then the expression of delayed hypersensitivity in vivo.
42  we show that using a rat model of cutaneous delayed hypersensitivity, MCP-1 expression correlates sp
43                   Three patients developed a delayed hypersensitivity reaction after vaccination.
44 histochemical findings suggest a mixed-type, delayed hypersensitivity reaction as the mechanism of in
45                                We describe a delayed hypersensitivity reaction to Jorveza(R), a newly
46 nd findings suggest that HORV is caused by a delayed hypersensitivity reaction to vancomycin.
47 ction rate is high, and it was produced by a delayed hypersensitivity reaction with a Th2 response.
48 through an indirect mechanism similar to the delayed hypersensitivity reaction.
49 ctions to the Moderna COVID-19 vaccine are a delayed hypersensitivity reaction.
50         The immunological mechanisms driving delayed hypersensitivity reactions (HSRs) to drugs media
51 osis, osteoporosis, as well as immediate and delayed hypersensitivity reactions (HSRs).
52 d in EPA and DHA suppressed antigen-specific delayed hypersensitivity reactions and mitogen-induced p
53                Currently, desensitization in delayed hypersensitivity reactions is restricted to mild
54 B1*10:01 was identified in 268 patients with delayed hypersensitivity reactions to B-lactams.
55 B1*10:01 was identified in 268 patients with delayed hypersensitivity reactions to beta-lactams.
56 dies report a very low incidence of acute or delayed hypersensitivity reactions to the antivenom.
57                                              Delayed hypersensitivity reactions were not predictive o
58                 Individuals with AGS develop delayed hypersensitivity reactions, with symptoms occurr
59                                          The delayed hypersensitivity response to intradermal tubercu
60                                              Delayed hypersensitivity response to purified protein de
61 taneously in two doses 2 weeks apart, evoked delayed hypersensitivity responses in a concentration-de
62                                              Delayed hypersensitivity responses were not significantl
63 method for inducing tolerance in humoral and delayed hypersensitivity responses which is associated w
64 atients) and healthy control subjects with a delayed hypersensitivity skin test response to M. avium
65 ripheral T-cell function, as measured by the delayed hypersensitivity skin test to tuberculin, and an
66                                              Delayed hypersensitivity to IRBP was marginally reduced,
67 ere was a strong inverse association between delayed hypersensitivity to Mycobacterium tuberculosis a
68 icantly associated with an increased risk of delayed hypersensitivity to penicillins (OR, 1.7; 95% CI
69 :02 alleles in the risk management of severe delayed hypersensitivity to penicillins should be evalua
70 ns and aztreonam in subjects with documented delayed hypersensitivity to penicillins who especially r
71                               Donor-specific delayed hypersensitivity was not detected at 12 days, bu
72                             We show that the delayed hypersensitivity was not mediated by either cell