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1 al specialized lymphoid microenvironments in secondary lymphoid tissue.
2 lammatory cytokines to mature and migrate to secondary lymphoid tissue.
3 homing receptors induced upon activation in secondary lymphoid tissue.
4 an tonsil was used as a positive control for secondary lymphoid tissue.
5 tial for the development and organization of secondary lymphoid tissue.
6 and kidneys does not require the presence of secondary lymphoid tissue.
7 sonable estimation of CTL in an individual's secondary lymphoid tissue.
8 ed during or after entry of lymphocytes into secondary lymphoid tissue.
9 e receptor normally required for egress from secondary lymphoid tissue.
10 plays a critical role in their movement into secondary lymphoid tissue.
11 r the earliest delivery of these bacteria to secondary lymphoid tissue.
12 ticle-associated HIV RNA in the follicles of secondary lymphoid tissue.
13 constitute most TCRgammadelta(+) T cells in secondary lymphoid tissue.
14 he upregulation of immunomodulatory genes in secondary lymphoid tissues.
15 culated continuously and dispersed widely to secondary lymphoid tissues.
16 rate to and expand in GVHD target organs and secondary lymphoid tissues.
17 tes and allowed the identification of RTE in secondary lymphoid tissues.
18 development of BM mNK cells, LTi cells, and secondary lymphoid tissues.
19 s, lymphoid tissue-inducing (LTi) cells, and secondary lymphoid tissues.
20 ew model of human NK cell differentiation in secondary lymphoid tissues.
21 ches, normal architecture and cellularity of secondary lymphoid tissues.
22 ators of the immune system and disruption of secondary lymphoid tissues.
23 ng from the thymus and recirculation through secondary lymphoid tissues.
24 cosal and peripheral sites to local draining secondary lymphoid tissues.
25 ion and reconstitution in murine primary and secondary lymphoid tissues.
26 sion of genes responsible for trafficking to secondary lymphoid tissues.
27 of interferon-gamma and interleukin 4 in the secondary lymphoid tissues.
28 t)CD16- NK cell subset, which is enriched in secondary lymphoid tissues.
29 VCAM-1, in marked contrast to HEVs in other secondary lymphoid tissues.
30 hes during activation and differentiation in secondary lymphoid tissues.
31 he embryonic development and organization of secondary lymphoid tissues.
32 depletion was profound in the periphery and secondary lymphoid tissues.
33 ific CD8+ T cells in the complete absence of secondary lymphoid tissues.
34 and their precursors in bone marrow (BM) and secondary lymphoid tissues.
35 CL21, chemokines expressed constitutively in secondary lymphoid tissues.
36 ection in mutant mice that lack all of their secondary lymphoid tissues.
37 ot generate memory T cells in mice devoid of secondary lymphoid tissues.
38 regulate the trafficking of T cells through secondary lymphoid tissues.
39 lpha4beta7 integrin-dependent trafficking to secondary lymphoid tissues.
40 en expressed by B-cell lymphomas residing in secondary lymphoid tissues.
41 nments, namely the T cell compartment of the secondary lymphoid tissues.
42 y dendritic cells within the T cell areas of secondary lymphoid tissues.
43 ction and microenvironmental localization in secondary lymphoid tissues.
44 es dendritic cell and T cell interactions in secondary lymphoid tissues.
45 signals outside the organized structures of secondary lymphoid tissues.
46 adult mouse is dependent on the presence of secondary lymphoid tissues.
47 ng in a decline in pDCs from circulation and secondary lymphoid tissues.
48 , as well as for organogenesis of thymic and secondary lymphoid tissues.
49 migrated to follicle proximal regions in all secondary lymphoid tissues.
50 DC originate from local stromal cells in the secondary lymphoid tissues.
51 ent distinct stages of B cell development in secondary lymphoid tissues.
52 in dendritic cells within the T cell zone of secondary lymphoid tissues.
53 tion of activated B cells into the T zone of secondary lymphoid tissues.
54 extravasation from the blood into organized secondary lymphoid tissues.
55 extravasation from the blood into organized secondary lymphoid tissues.
56 thymocytes and restricted to T cell areas in secondary lymphoid tissues.
57 ompared with extrafollicular (EF) regions of secondary lymphoid tissues.
58 be generated in the complete absence of all secondary lymphoid tissues.
59 ells and activation of lymphoid follicles in secondary lymphoid tissues.
60 t induces their migration to the recipient's secondary lymphoid tissues.
61 influence on IL-7 amounts in the primary and secondary lymphoid tissues.
62 orchestrate the generation and maturation of secondary lymphoid tissues.
63 d activation and effector differentiation in secondary lymphoid tissues.
64 al natural killer (cNK) cells are present in secondary lymphoid tissues.
65 diminished function of mature lymphocytes in secondary lymphoid tissues.
66 6C(high) monocytes in the circulation and in secondary lymphoid tissues.
67 ls and DCs, resulting in their entrapment in secondary lymphoid tissues.
68 ally within the lamina propria but not other secondary lymphoid tissues.
69 st fall in recent CD4(+) thymic emigrants in secondary lymphoid tissues.
70 or CLL cells preferentially proliferating in secondary lymphoid tissues.
71 mphoplastic (aly/aly) recipients, which lack secondary lymphoid tissues.
72 uctures within the follicular regions of the secondary lymphoid tissues.
73 topoietic cells interact within conventional secondary lymphoid tissues.
74 peripheral sites of inflammation and remote secondary lymphoid tissues.
75 e-specific CD8(+)IFN-gamma(+) T cells in the secondary lymphoid tissues.
76 Similar observations were noted in the secondary lymphoid tissues.
77 for manipulation of liver DC trafficking to secondary lymphoid tissue after liver transplantation.
78 nutes in all antigen-specific CD4 T cells in secondary lymphoid tissues after injection of peptide an
79 elper and T effector cells to be retained in secondary lymphoid tissue and away from sites of inflamm
81 cient localization of naive T lymphocytes to secondary lymphoid tissue and constitutive recirculation
82 es many of the functional characteristics of secondary lymphoid tissue and contains autoantibody-secr
83 ells from the lung airways can return to the secondary lymphoid tissue and respond to a secondary vir
84 T cell stimulation and proliferation in the secondary lymphoid tissue and, on the other hand, to the
85 a high frequency of apoptotic lymphocytes in secondary lymphoid tissues and a macrophage defect in ap
86 rably less immunostimulatory than those from secondary lymphoid tissues and are equipped to promote i
87 ary Cryptococcus neoformans infection in the secondary lymphoid tissues and at the site of primary in
88 y T cells (TCM), which are restricted to the secondary lymphoid tissues and blood, and effector memor
89 CD4+ T lymphocytes from peripheral blood and secondary lymphoid tissues and died within the first 6 m
90 hroughout the natural course of infection in secondary lymphoid tissues and in particular within the
91 of lymphocyte subpopulations in primary and secondary lymphoid tissues and in the recruitment of leu
92 transferred allogeneic HSCs migrated to the secondary lymphoid tissues and induced Treg expansion in
93 n potentially migrate to the B cell areas of secondary lymphoid tissues and suppress T cell-dependent
94 r switches of FoxP3(+) T cells in thymus and secondary lymphoid tissues and the functional consequenc
95 ules, is involved both in the development of secondary lymphoid tissues and the maintenance of organi
96 the basal migration of RDC from the lungs to secondary lymphoid tissues and their enhanced maturation
97 ndergo activation in the T cell-rich zone of secondary lymphoid tissues and then migrate to B cell ar
99 on is an active process that operates beyond secondary lymphoid tissue, and involves the persistent p
101 the frequency of secondary CD8(+) T cells in secondary lymphoid tissues, and can be accounted for by
103 alpha4beta1 integrin/VCAM-1 is unique among secondary lymphoid tissues, and may help unify lymphocyt
104 he frequency of T regulatory (T(R)) cells in secondary lymphoid tissues, and regulates T(R) cell chem
105 Because TNF-alpha signaling is critical for secondary lymphoid tissue architecture, we examined comp
106 or the development and maintenance of proper secondary lymphoid tissue architecture; however, the und
108 chronic inflammation, structures that mimic secondary lymphoid tissues are observed, suggesting that
110 ls, TFH, residing in B-cell follicles within secondary lymphoid tissues, are readily infected by AIDS
111 al activation of autoreactive lymphocytes in secondary lymphoid tissue, as this is equally relevant t
112 ated with blockade of lymphocyte egress from secondary lymphoid tissue, as well as with more generali
113 spond to the medullary stroma-expressed (and secondary lymphoid tissue-associated) chemokines seconda
114 nctions, including roles in the formation of secondary lymphoid tissues at early time points during t
115 with the anamnestic response, the ability of secondary lymphoid tissue-based (central) memory T cells
116 king AhR demonstrate reduced accumulation in secondary lymphoid tissue because of low levels of proli
117 epertoire, no differences were seen in three secondary lymphoid tissues between piglets lacking IPP a
118 ll dysregulation in the peripheral blood and secondary lymphoid tissues, bone marrow plasma cells rem
119 llicular IFN-gamma+ CD8 T cells were rare in secondary lymphoid tissues but accounted for the majorit
120 g molecule not only for the organogenesis of secondary lymphoid tissues but for the maintenance of as
121 sable for dendritic cell (DC) homeostasis in secondary lymphoid tissues but necessary to regulate cel
122 3(+) thymic emigrants migrate exclusively to secondary lymphoid tissues but poorly to nonlymphoid tis
123 lymphocytic leukemia (CLL) cells multiply in secondary lymphoid tissue, but the mechanisms leading to
124 anted organs without the need for priming in secondary lymphoid tissues, but the mechanisms by which
125 The regulation of T-cell trafficking in secondary lymphoid tissues by CCL21 is therefore a tight
126 nductive phase of the immune response in the secondary lymphoid tissues by IL-10-independent mechanis
127 temperatures stimulate lymphocyte homing to secondary lymphoid tissues by increasing L-selectin and
128 that circulating CLL cells and those within secondary lymphoid tissues can make AID mRNA and protein
130 to the CC chemokine receptor (CCR)7 ligands secondary lymphoid tissue chemoattractant (SLC) and macr
131 n segments displaying high levels of luminal secondary lymphoid tissue chemokine (SLC) (6Ckine, Exodu
133 e expression of thymic medullary chemokines (secondary lymphoid tissue chemokine (SLC) and EBV-induce
134 pha), thymus-expressed chemokine (TECK), and secondary lymphoid tissue chemokine (SLC) but not of oth
135 cells (DCs) genetically modified to express secondary lymphoid tissue chemokine (SLC) into growing B
141 emotactic responses of LPS-stimulated DCs to secondary lymphoid tissue chemokine (SLC)/CC chemokine l
143 implicated particularly in T-cell movement, secondary lymphoid tissue chemokine (SLC, CCL21) and Eps
144 HEV-decorated homeostatic chemokines such as secondary lymphoid tissue chemokine (SLC; CCL21) to its
145 press CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-
146 lecules, including the chemotactic molecules secondary lymphoid tissue chemokine and Fas ligand and t
148 transgenic mice with mice expressing CCL21 (secondary lymphoid tissue chemokine) revealed that CCL21
149 of thymus-derived chemotactic agent (TCA)-4 (secondary lymphoid tissue chemokine, 6Ckine, Exodus-2) i
150 n 1, macrophage inflammatory protein 1 beta, secondary lymphoid tissue chemokine, and interleukin 8)
151 immature DC, but not homeostatic chemokines secondary lymphoid tissue chemokine, CCL21, or stromal c
152 and activation-regulated chemokine/CCL17 or secondary lymphoid tissue chemokine/CCL21, caused a 50-7
157 (TARC), C10), and d) constitutive (lungkine, secondary lymphoid-tissue chemokine (SLC), EBI1-ligand c
158 a chemokine represented in the EST database, secondary lymphoid-tissue chemokine (SLC), is expressed
160 6), and regulatory chemokine receptors CCR7 (secondary lymphoid-tissue chemokine (SLC)/CC ligand (CCL
161 ndary lymphoid tissue-associated) chemokines secondary lymphoid-tissue chemokine and macrophage infla
162 ctivation-regulated chemokine) and CCR7 (for secondary lymphoid-tissue chemokine and macrophage infla
163 s, macrophage inflammatory protein 3beta and secondary lymphoid-tissue chemokine significantly (P < 0
164 ogenic signaling pathways, and that--outside secondary lymphoid tissues--clonal evolution is retarded
165 arily reside in nonlymphoid tissues, whereas secondary lymphoid tissues contain functionally quiescen
166 omal derived factor 1 alpha [SDF-1 alpha] or secondary lymphoid tissue cytokine), and ERM proteins lo
168 h congenital defects in different aspects of secondary lymphoid tissue development are beginning to c
169 s, now recognized to be essential for normal secondary lymphoid tissue development, is also a feature
170 xpression of mature DC-specific marker CD83, secondary lymphoid tissue-directing chemokine receptor C
171 racrine IL-2 produced in the T cell zones of secondary lymphoid tissues due to their expression of th
172 within CD4(+) T cells in B cell follicles of secondary lymphoid tissues during asymptomatic disease.
173 t T-cell activation and effector function in secondary lymphoid tissues during fungal infection is ch
175 we find expression of H(1gj) in primary and secondary lymphoid tissues early in life, but in adults
176 phocyte trafficking, the BM can supplant the secondary lymphoid tissue either as a site of primary im
177 ntation and the increased APC recruitment to secondary lymphoid tissues expand the scope of known adj
179 y to transport antigen from the periphery to secondary lymphoid tissues for the activation of naive T
180 induced mouse plasmacytomas were detected in secondary lymphoid tissues from normal mice, chiefly in
181 itative imaging in mice to show that, within secondary lymphoid tissues, highly suppressive Treg cell
182 go chemokine receptor switch from CD45RA(+) (secondary lymphoid tissue homing) to CD45RO(+) type (lym
183 expansion of tumor-specific CD8+ T cells in secondary lymphoid tissue; however, CD8+ T cells that ha
184 g Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic
185 tivation and proliferation of lymphocytes in secondary lymphoid tissue in response to infection.
186 XCL9/monokine induced by gamma interferon in secondary lymphoid tissue in SIV infection, no differenc
187 en-specific T-cell abundance was observed in secondary lymphoid tissues in either acute or persistent
188 s patches (PPs) are unique compared to other secondary lymphoid tissues in their continual exposure t
189 olved in the development and organization of secondary lymphoid tissues, in the pathogenesis of EAE.
190 ed with B(Mem) frequency differences between secondary lymphoid tissues indicating an influence of lo
191 ted indefinitely in recipient mice that lack secondary lymphoid tissue, indicating that the alloimmun
192 e lymphoid and nonlymphoid components of the secondary lymphoid tissues, information concerning the s
194 ulations of the immune compartment, and that secondary lymphoid tissue is anatomically poised to be r
198 e-directed homing of donor dendritic cell to secondary lymphoid tissues is essential for host sensiti
199 Movement of T and B lymphocytes through secondary lymphoid tissues is likely to involve multiple
200 +) Tregs early but not late postinfection in secondary lymphoid tissues is more efficacious in contro
201 The number of B lymphocytes in primary and secondary lymphoid tissues is normal in B7.2 transgenic
204 trate that SPAG6 is expressed in primary and secondary lymphoid tissues, is associated with the centr
205 +) T cells have been identified in different secondary lymphoid tissues, it is not known which subpop
206 ally resident T cells and those that entered secondary lymphoid tissue later were primed in very diff
208 rprisingly, in spite of the severe defect in secondary lymphoid tissue, LTalpha(-/-) mice could clear
211 id tissue induced by TMPD not only resembles secondary lymphoid tissue morphologically, but it also d
213 o homing of DC from peripheral s.c. sites to secondary lymphoid tissue of syngeneic or allogeneic rec
215 type and cytokine patterns in the thymus and secondary lymphoid tissues of FIV-infected cats were inv
218 upregulated in intestinal effector sites and secondary lymphoid tissues of intranasally immunized BAL
222 iTreg generation and function is limited to secondary lymphoid tissue or whether it can occur within
223 s that are specialized to proliferate in the secondary lymphoid tissues or to fight infection at the
224 ese observations can be generalized to other secondary lymphoid tissues or whether virus compartmenta
225 ered to the CD8+ cells during priming within secondary lymphoid tissues, or alternatively is due to t
226 (CTL) differentiation, whereas CD8 cells in secondary lymphoid tissue proliferated but were not cyto
227 ncing the formation of memory CD8 T cells in secondary lymphoid tissues, rapamycin inhibits the forma
228 r T cells were those that initially targeted secondary lymphoid tissue, rather than tumor sites, as h
229 emory cell reconstitution lags behind a slow secondary lymphoid tissue recovery, with important impli
230 ory preferences of memory cells dictated the secondary lymphoid tissue requirement for the recall res
233 a cells: short-lived ones that appear in the secondary lymphoid tissue shortly after Ag exposure, and
234 d NK-22 cells, was recently described within secondary lymphoid tissue (SLT) as IL-22(-) when resting
235 an natural killer (NK) cell intermediates in secondary lymphoid tissue (SLT), stage 3 CD34(-)CD117(+)
239 identified a progenitor population in human secondary lymphoid tissues (SLTs) that expressed the tra
241 hogen, engulf and traffic foreign antigen to secondary lymphoid tissues, stimulating antigen-specific
244 inusoids of the liver and only 5% migrate to secondary lymphoid tissues such as lymph nodes, Peyer's
246 A was shown to be predominantly expressed in secondary lymphoid tissues, such as lymph node, spleen,
248 en (Ag) in peripheral tissues and migrate to secondary lymphoid tissues, such as lymph nodes (LNs), w
249 and clustering of circulating leukocytes to secondary lymphoid tissues, such as lymph nodes and Peye
251 t and respond to foreign Ag independently of secondary lymphoid tissues supports the existence of non
252 etric analyses of CD8+ T cells isolated from secondary lymphoid tissue that revealed a phenotypic pro
253 Although CD4(+) memory T cells reside within secondary lymphoid tissue, the major reservoir of these
254 sence of a functional ER was demonstrated in secondary lymphoid tissues, then ERalpha expression was
255 ting cells, proliferate and differentiate in secondary lymphoid tissues, then traffic to the infected
256 s and facilitates their rapid sequester into secondary lymphoid tissues, thereby regulating the accum
257 ive vaccine should prevent infection of this secondary lymphoid tissue; therefore, the potential of a
258 c lymphoid tissue morphologically resembling secondary lymphoid tissues, though it is unclear whether
260 esize that IL-2 can mobilize the NK cells of secondary lymphoid tissues to mediate natural killing du
261 in NOD mice do not require the morphology of secondary lymphoid tissues to support their role in dise
262 ve T cells predominantly recirculate through secondary lymphoid tissue until antigen encounter, while
263 ive T cells continuously recirculate between secondary lymphoid tissue via the blood and lymphatic sy
266 at the expansion of antiviral CD8 T cells in secondary lymphoid tissues was IL-2 independent, whereas
267 drug FTY720 leads to trapping of T cells in secondary lymphoid tissues, we evaluated the possibility
268 I+ DC progenitors that migrated to recipient secondary lymphoid tissue were cells that appeared to ha
270 LTi) cells and mouse adult LTi-like cells in secondary lymphoid tissues were found to release IL-22,
272 HEV are blood vessels normally found in secondary lymphoid tissue where they are specialized for
273 lls (FDCs) reside within germinal centers of secondary lymphoid tissue where they play a critical rol
274 nonmalignant cells within pseudofollicles in secondary lymphoid tissue where tumor cell proliferation
275 the TTSS to rapidly drive respiratory DCs to secondary lymphoid tissues where these APCs stimulate an
276 irculating memory B cells frequently reenter secondary lymphoid tissue, where they receive signals es
277 ady state and after liver transplantation to secondary lymphoid tissues, where the outcome of their i
279 taneously acquired memory-like properties in secondary lymphoid tissues, where tumor antigen level re
280 naive CD4+ T cells from peripheral blood and secondary lymphoid tissues, which declined at rates that
281 rm across both the T cell repertoire and the secondary lymphoid tissues, while (ii) retaining toleran
282 A polymerase, is preferentially expressed in secondary lymphoid tissues with yet unknown physiologica
283 Donor dendritic cells rapidly migrated into secondary lymphoid tissues within 3 h of transplantation
284 sAg) and membrane-associated Ag (mAg) in the secondary lymphoid tissue, yet how the physical form of
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