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1 e of MHC-peptide antigen presentation to the alpha beta T cell.
2 ontogeny and occurs in both gamma delta and alpha beta T cells.
3 ed by gene targeting so that these mice lack alpha beta T cells.
4 gnificantly augmented by as few as 1 x 10(5) alpha beta T cells.
5 and secondary sites, and is mediated by CD8+ alpha beta T cells.
6 ction have drawn heavily on our knowledge of alpha beta T cells.
7 pus-prone MRL mice congenitally deficient in alpha beta T cells.
8 ut they do so in a way that is distinct from alpha beta T cells.
9 important for the subsequent development of alpha beta T cells.
10 cells while retaining normal frequencies of alpha beta T cells.
11 delta subset of T cells, which may regulate alpha beta T cells.
12 to ligands that are different from those of alpha beta T cells.
13 may not recognize antigen the same way as do alpha beta T cells.
14 o primary infection as mice deficient in all alpha beta T cells.
15 ied by an increase in the percentage of CD4+ alpha beta T cells.
16 V beta usage during T. gondii stimulation of alpha beta T cells.
17 e infection with C. parvum was restricted to alpha/beta T cells.
18 could be induced in gamma/delta T cells and alpha/beta T cells.
19 ecrosis in the ilea after infection are CD4+ alpha/beta T cells.
20 dependent on the collaboration between B and alpha/beta T cells.
21 lpha-/- mice that are congenitally devoid of alpha/beta T cells.
22 IEL were up-regulated in the presence of TCR(alpha beta) T cells.
23 proliferation of normal gamma delta, but not alpha beta, T cells.
24 of diseased recipients are host-derived CD4+ alpha/beta+ T cells.
27 cells share many cell surface proteins with alpha beta T cells and are able to secrete lymphokines a
29 Cytokine signaling by IL-2 and IL-7 from alpha beta T cells and epithelial cells was necessary fo
30 or suppressor, and identifies roles for both alpha beta T cells and gamma delta T cells in Fas-indepe
33 of the magnitude of major superantigens for alpha beta T cells and may bridge the gap between innate
34 ay inflammation, mediated by accumulation of alpha/beta T cells and driven by DCs, is critical to air
36 the ligand for Fas (APO-1, CD95) compared to alpha beta T cells, and induce apoptosis of Fashigh CD4+
37 ing for activated macrophages, the number of alpha beta T cells, and the number of delta gamma epithe
38 with elevated numbers of NK cell, NKT cell, alpha/beta T cell, and macrophage infiltration of the in
39 E alpha 52-68/I-A(b) complex-specific 1H3.1 alpha beta T cell antigen receptor are positively select
43 lized autoimmunity, but autoantigen-specific alpha beta T cells are required to cause overt disease.
44 eficiency, suggesting that CD4(+) and CD8(+) alpha/beta(+) T cells are sufficient to mount a protecti
46 ll maturation was strictly restricted to TCR-alpha beta T cells as the absolute number of thymic dend
47 lly share many common features with adaptive alpha/beta T cells, as both lineages include naive-like
48 n of activated gamma delta T cells and naive alpha beta T cells at the time of bone marrow transplant
49 the interleukin 7 receptor (IL-7R) generate alpha/beta T cells at a detectable but greatly reduced r
50 ifically stained gamma delta T cells and not alpha beta T cells, B cells, neutrophils, or monocytes.
51 d in substantial increases in the numbers of alpha/beta T cells, both CD4+ (150%) and CD8+ (60%), and
53 igher ratios of gamma/delta T cells and CD4+ alpha/beta T cells but lower ratios of CD8+ alpha/beta T
54 rial Ag is dependent on the presence of CD4+ alpha beta T cells, but the requirement for CD4+ alpha b
57 ere rendered deficient in CD40 ligand and/or alpha beta T cells by intercrossing CD40L -/- and TCR-al
58 a beta T cells, but the requirement for CD4+ alpha beta T cells can be met by cytokines that use the
59 ld-type or mutant mice shows that 65% of all alpha/beta T cells carry receptors that are normally ass
61 alpha/beta T cells but lower ratios of CD8+ alpha/beta T cells compared to those of infected IL-6(-/
62 mma delta T cells was inhibited by an intact alpha beta T cell compartment, and both populations were
67 t or anti-CD20 B cell-depleted mice, but not alpha/beta T cell-deficient mice, display decreased infl
68 ncluding that MRL autoimmunity requires CD4+ alpha beta T cells, demonstrate that non-alpha beta T ce
69 chanism; 2) identify a role for CD40L in non-alpha beta T cell-dependent autoantibody production and
70 D4+ alpha beta T cells, demonstrate that non-alpha beta T cell-dependent mechanisms are capable of in
72 gs demonstrating a role for CD40L-dependent, alpha beta T cell-dependent mechanisms in autoantibody p
74 nd Fyn (lck(-/-)fyn(-/-)) completely arrests alpha beta T cell development at the CD4-CD8- stage.
75 ion of Bcl-2 in these mice partially rescued alpha beta T cell development but not gamma delta T cell
76 The ability of CD16 cross-linking to block alpha beta T cell development was not attributable to to
77 "beta selection." This is the first point in alpha beta T-cell development at which the products of a
80 Lck and Fyn in the absence of Csk uncouples alpha/beta T cell development entirely from engagement o
81 provide genetic evidence for this notion as alpha/beta T cell development is blocked in lck(-/)-fyn(
82 ic organ cultures from Lef1-/- Tcf1-/- mice, alpha/beta T cell differentiation is completely arrested
83 esponse to Eimeria vermiformis, mice lacking alpha beta T cells display defects in protective immunit
84 gly, the requirements for a highly effective alpha beta-T-cell-driven memory response are less string
85 differentiation, and expansion of mainstream alpha/beta T cells during ontogeny depend on the highly
89 tions, 80% of gamma/delta T cells and 53% of alpha/beta T cells formed shear-resistant adhesions to P
90 tro reactivity to Toxoplasma gondii of human alpha beta T cells from T. gondii-seronegative individua
91 (CD45RO+) phenotypes from adults as well as alpha beta T cells from T. gondii-seronegative newborns
94 ese data show that, whereas less potent than alpha beta T cells, gamma delta T cells are able to prom
95 cells in vitro; however, in contrast to CD4+ alpha beta T cells, gamma delta T cells predominantly pr
98 alpha/beta and that the Vbeta1 subset of TCR alpha/beta T cells had a dominant role in protective imm
100 t ultimately populate the thymus to generate alpha/beta T cells has been controversial, and their mol
104 n distinguishes gamma delta T cell help from alpha beta T cell help induced under analogous circumsta
107 ncluding autoantibodies) is a product of non-alpha/beta T cell help that can be provided by gamma/del
111 that gamma delta T cells can substitute for alpha beta T cells in a virus model of demyelination and
112 oimmune disease, and to address the roles of alpha beta T cells in murine lupus, we analyzed lupus-pr
113 e graft-vs-host (GVH) reactivity mediated by alpha beta T cells in murine recipients transplanted wit
114 mune skin disease; and 3) suggest a role for alpha beta T cells in the down-regulation of autoimmunit
117 the forces driving polyclonal activation of alpha/beta T cells in lupus is an intrinsically heighten
118 d from the low numbers of CD8alpha/alpha TCR-alpha/beta T cells in mice deficient in Qa-2 genes.
119 an eightfold increase in the CD8+, Db/HY TCR-alpha/beta T cells in the lymph nodes (LN) of delta Nur7
120 the other subsets to naive and memory CD8(+) alpha/beta T cells, in this study, we show that Ly-6C(-
121 transfer of various populations of B and non-alpha/beta T cells including cloned gamma/delta T cells
122 suggest that MRL disease may consist of both alpha beta T cell-independent and alpha beta T cell-depe
123 D4(+) T (NKT) cells, gamma/delta T cells, or alpha/beta T cells indicated that alpha/beta CD4(+) T ce
124 MC completely abrogated the proliferation of alpha beta T cells, indicating the need for processing o
126 40L-intact or -deficient (CD40L+ or CD40L-), alpha beta T cell-intact or -deficient (alpha beta+ or a
132 genic reporter delta deletion construct show alpha/beta T cell lineage-specific use of the transgenic
133 The developmental block is specific to the alpha/beta T-cell lineage at a stage before the completi
134 delta genes were deleted on both alleles in alpha beta T cell lines, thereby indicating conservation
137 lass of antigens, lipids and glycolipids, to alpha/beta T cells, little is known about the T cell sub
140 n murine lupus, they also: 1) establish that alpha beta T cells may drive autoimmune skin disease by
143 r beta 2m 0/0 knockout mice, which lack CD8+ alpha beta T cells, nor C57BL/6 mice depleted of CD8+ T
144 tive and -negative selection of conventional alpha beta T cells occur in anatomically distinct sites
145 d that contained only a single population of alpha beta T cells of foreign specificity by generating
148 ise homologues of the subset of NK1.1(+) TCR-alpha/beta+ T cells, often referred to as NK T cells, wh
150 ell-deficient mice, unlike mice deficient in alpha beta T cells or B cells, show no severe defects in
154 Generation of gamma/delta and of CD4-8- alpha/beta T cells proceeds normally despite blockade of
155 urified CD4+ alpha beta T cells but not CD8+ alpha beta T cells proliferated in response to these T.
158 mined for full-length and truncated forms of alpha beta T cell receptor (TCR) heterodimers, both alon
159 he specificity of a T cell is dictated by an alpha beta T cell receptor (TCR) that recognizes a compl
161 were either CD4+ or CD4+/CD8+, expressed the alpha beta T cell receptor, secreted IFN-gamma, and were
163 with monoclonal antibodies directed against alpha beta T-cell receptor (TCR)+, CD5+, and CD8+ T-cell
167 uced in the thymus, each expressing a unique alpha/beta T cell receptor (TCR) capable of binding to a
169 requirements for inducing downregulation of alpha/beta T cell receptor (TCR) molecules on naive majo
171 ority of CD8(+) cells do not express surface alpha/beta T cell receptor alpha/beta(TCR), gamma/deltaT
175 ty (85%) of CD3+ VL are CD4+ and express the alpha/beta T-cell receptor (TCR), similar to the results
178 iated with a reduced infiltration of CD8 and alpha/beta T-cell receptor-expressing cells, diminished
181 se lines revealed > 99% CD3+, 85 to 95% CD3+ alpha beta T-cell-receptor-positive (TCR+), 5 to 9% CD3+
184 ative T cells" (DNTs), T lymphocytes bearing alpha beta T cell receptors and expressing neither clust
185 tural killer-1+ natural T cells that express alpha beta T cell receptors requires a conserved beta 2-
188 These NC16A-responding T lymphocytes express alpha/beta T cell receptors and CD4 memory T cell surfac
189 rther supports the idea that gamma delta and alpha beta T cells recognize antigens differently and su
190 to control L. major, mice with a monoclonal alpha beta T cell repertoire (ABLE TCR-C alpha 0 mice) d
192 n of gamma delta T cell replenishment before alpha beta T cell reseeding, thereby indicating the comp
198 f autoimmune diseases with only autoreactive alpha beta T cells seem invariably to fall short for lac
205 s effect indirectly through donor BM-derived alpha beta T cells that acted as the proximate regulator
206 NK1 T cells are a specialized population of alpha/beta T cells that coexpress receptors of the NK li
207 1+ (NK1) T cells are a specialized subset of alpha/beta T cells that coexpress surface receptors that
209 g-term surviving mouse kidney allografts are alpha/beta-T cells that have downregulated their cell su
211 e cells are derived from mature autoreactive alpha/beta T cells, the significance of coreceptor downr
212 aracterized collaboration between B and "non-alpha/beta T" cells, the phenotype has been reconstitute
213 the ability of MHC-incompatible nontolerant alpha beta T cells to cause GVHD after allogeneic BMT.
214 e able to signal the migration of peripheral alpha beta T cells to the epidermis by secreting specifi
215 e stimuli, though promoting the expansion of alpha beta-T cells, usually do not promote the efficient
216 electin glycoprotein ligand (PSGL-1), as all alpha/beta T cells versus approximately 75% of gamma/del
217 n contrast, when the administration of naive alpha beta T cells was delayed for 2 wk post-BMT, surviv
218 at fetal day 16.5 and is strictly limited to alpha beta T cells, we find that rearrangement under the
219 roperty of gamma delta T cells, as activated alpha beta T cells were incapable of ameliorating the su
220 aftment, indicating that limiting numbers of alpha beta T cells were required in the marrow graft for
221 In contrast, mice specifically lacking only alpha beta-T cells were no more susceptible than wild-ty
223 These cells, but not conventional CD4 or CD8 alpha beta T cells, were detected in the central nervous
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