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1 r the earliest delivery of these bacteria to secondary lymphoid tissue.
2 ticle-associated HIV RNA in the follicles of secondary lymphoid tissue.
3 constitute most TCRgammadelta(+) T cells in secondary lymphoid tissue.
4 al specialized lymphoid microenvironments in secondary lymphoid tissue.
5 lammatory cytokines to mature and migrate to secondary lymphoid tissue.
6 homing receptors induced upon activation in secondary lymphoid tissue.
7 an tonsil was used as a positive control for secondary lymphoid tissue.
8 tial for the development and organization of secondary lymphoid tissue.
9 and kidneys does not require the presence of secondary lymphoid tissue.
10 sonable estimation of CTL in an individual's secondary lymphoid tissue.
11 ed during or after entry of lymphocytes into secondary lymphoid tissue.
12 e receptor normally required for egress from secondary lymphoid tissue.
13 plays a critical role in their movement into secondary lymphoid tissue.
14 e-specific CD8(+)IFN-gamma(+) T cells in the secondary lymphoid tissues.
15 Similar observations were noted in the secondary lymphoid tissues.
16 he upregulation of immunomodulatory genes in secondary lymphoid tissues.
17 culated continuously and dispersed widely to secondary lymphoid tissues.
18 rate to and expand in GVHD target organs and secondary lymphoid tissues.
19 tes and allowed the identification of RTE in secondary lymphoid tissues.
20 development of BM mNK cells, LTi cells, and secondary lymphoid tissues.
21 s, lymphoid tissue-inducing (LTi) cells, and secondary lymphoid tissues.
22 influence on IL-7 amounts in the primary and secondary lymphoid tissues.
23 ew model of human NK cell differentiation in secondary lymphoid tissues.
24 ches, normal architecture and cellularity of secondary lymphoid tissues.
25 ng from the thymus and recirculation through secondary lymphoid tissues.
26 ion and reconstitution in murine primary and secondary lymphoid tissues.
27 sion of genes responsible for trafficking to 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 es a systemic immune response in primary and secondary lymphoid tissues.
37 ection in mutant mice that lack all of their secondary lymphoid tissues.
38 ot generate memory T cells in mice devoid of secondary lymphoid tissues.
39 regulate the trafficking of T cells through secondary lymphoid tissues.
40 lpha4beta7 integrin-dependent trafficking to secondary lymphoid tissues.
41 en expressed by B-cell lymphomas residing in secondary lymphoid tissues.
42 nments, namely the T cell compartment of the secondary lymphoid tissues.
43 y dendritic cells within the T cell areas of secondary lymphoid tissues.
44 ction and microenvironmental localization in secondary lymphoid tissues.
45 es dendritic cell and T cell interactions in secondary lymphoid tissues.
46 signals outside the organized structures of secondary lymphoid tissues.
47 adult mouse is dependent on the presence of secondary lymphoid tissues.
48 ators of the immune system and disruption of secondary lymphoid tissues.
49 cosal and peripheral sites to local draining secondary lymphoid tissues.
50 migrated to follicle proximal regions in all secondary lymphoid tissues.
51 of interferon-gamma and interleukin 4 in the secondary lymphoid tissues.
52 DC originate from local stromal cells in the secondary lymphoid tissues.
53 ent distinct stages of B cell development in secondary lymphoid tissues.
54 in dendritic cells within the T cell zone of secondary lymphoid tissues.
55 tion of activated B cells into the T zone of secondary lymphoid tissues.
56 extravasation from the blood into organized secondary lymphoid tissues.
57 extravasation from the blood into organized secondary lymphoid tissues.
58 thymocytes and restricted to T cell areas in secondary lymphoid tissues.
59 oluble molecules that interact with maternal secondary lymphoid tissues.
60 ng in a decline in pDCs from circulation and secondary lymphoid tissues.
61 , as well as for organogenesis of thymic and secondary lymphoid tissues.
62 ompared with extrafollicular (EF) regions of secondary lymphoid tissues.
63 be generated in the complete absence of all secondary lymphoid tissues.
64 ells and activation of lymphoid follicles in secondary lymphoid tissues.
65 t induces their migration to the recipient's secondary lymphoid tissues.
66 orchestrate the generation and maturation of secondary lymphoid tissues.
67 d activation and effector differentiation in secondary lymphoid tissues.
68 al natural killer (cNK) cells are present in secondary lymphoid tissues.
69 diminished function of mature lymphocytes in secondary lymphoid tissues.
70 6C(high) monocytes in the circulation and in secondary lymphoid tissues.
71 ls and DCs, resulting in their entrapment in secondary lymphoid tissues.
72 ally within the lamina propria but not other secondary lymphoid tissues.
73 st fall in recent CD4(+) thymic emigrants in secondary lymphoid tissues.
74 or CLL cells preferentially proliferating in secondary lymphoid tissues.
75 mphoplastic (aly/aly) recipients, which lack secondary lymphoid tissues.
76 uctures within the follicular regions of the secondary lymphoid tissues.
77 topoietic cells interact within conventional secondary lymphoid tissues.
78 peripheral sites of inflammation and remote secondary lymphoid tissues.
79 for manipulation of liver DC trafficking to secondary lymphoid tissue after liver transplantation.
80 nutes in all antigen-specific CD4 T cells in secondary lymphoid tissues after injection of peptide an
81 elper and T effector cells to be retained in secondary lymphoid tissue and away from sites of inflamm
83 cient localization of naive T lymphocytes to secondary lymphoid tissue and constitutive recirculation
84 es many of the functional characteristics of secondary lymphoid tissue and contains autoantibody-secr
85 ells from the lung airways can return to the secondary lymphoid tissue and respond to a secondary vir
86 T cell stimulation and proliferation in the secondary lymphoid tissue and, on the other hand, to the
87 a high frequency of apoptotic lymphocytes in secondary lymphoid tissues and a macrophage defect in ap
88 rably less immunostimulatory than those from secondary lymphoid tissues and are equipped to promote i
89 ary Cryptococcus neoformans infection in the secondary lymphoid tissues and at the site of primary in
90 y T cells (TCM), which are restricted to the secondary lymphoid tissues and blood, and effector memor
92 CD4+ T lymphocytes from peripheral blood and secondary lymphoid tissues and died within the first 6 m
93 hroughout the natural course of infection in secondary lymphoid tissues and in particular within the
94 of lymphocyte subpopulations in primary and secondary lymphoid tissues and in the recruitment of leu
95 transferred allogeneic HSCs migrated to the secondary lymphoid tissues and induced Treg expansion in
96 n potentially migrate to the B cell areas of secondary lymphoid tissues and suppress T cell-dependent
97 r switches of FoxP3(+) T cells in thymus and secondary lymphoid tissues and the functional consequenc
98 ules, is involved both in the development of secondary lymphoid tissues and the maintenance of organi
99 e CXCL13 controls the normal organization of secondary lymphoid tissues and the neogenesis of ectopic
100 the basal migration of RDC from the lungs to secondary lymphoid tissues and their enhanced maturation
101 ndergo activation in the T cell-rich zone of secondary lymphoid tissues and then migrate to B cell ar
103 on is an active process that operates beyond secondary lymphoid tissue, and involves the persistent p
105 the frequency of secondary CD8(+) T cells in secondary lymphoid tissues, and can be accounted for by
107 alpha4beta1 integrin/VCAM-1 is unique among secondary lymphoid tissues, and may help unify lymphocyt
108 he frequency of T regulatory (T(R)) cells in secondary lymphoid tissues, and regulates T(R) cell chem
109 Because TNF-alpha signaling is critical for secondary lymphoid tissue architecture, we examined comp
110 or the development and maintenance of proper secondary lymphoid tissue architecture; however, the und
112 chronic inflammation, structures that mimic secondary lymphoid tissues are observed, suggesting that
114 ls, TFH, residing in B-cell follicles within secondary lymphoid tissues, are readily infected by AIDS
115 al activation of autoreactive lymphocytes in secondary lymphoid tissue, as this is equally relevant t
116 ated with blockade of lymphocyte egress from secondary lymphoid tissue, as well as with more generali
117 spond to the medullary stroma-expressed (and secondary lymphoid tissue-associated) chemokines seconda
118 nctions, including roles in the formation of secondary lymphoid tissues at early time points during t
119 with the anamnestic response, the ability of secondary lymphoid tissue-based (central) memory T cells
120 king AhR demonstrate reduced accumulation in secondary lymphoid tissue because of low levels of proli
121 epertoire, no differences were seen in three secondary lymphoid tissues between piglets lacking IPP a
122 ll dysregulation in the peripheral blood and secondary lymphoid tissues, bone marrow plasma cells rem
123 llicular IFN-gamma+ CD8 T cells were rare in secondary lymphoid tissues but accounted for the majorit
124 g molecule not only for the organogenesis of secondary lymphoid tissues but for the maintenance of as
125 sable for dendritic cell (DC) homeostasis in secondary lymphoid tissues but necessary to regulate cel
126 3(+) thymic emigrants migrate exclusively to secondary lymphoid tissues but poorly to nonlymphoid tis
127 lymphocytic leukemia (CLL) cells multiply in secondary lymphoid tissue, but the mechanisms leading to
128 unlike Ig/TCR, the gene is not expressed in secondary lymphoid tissues, but mainly in the liver.
129 anted organs without the need for priming in secondary lymphoid tissues, but the mechanisms by which
130 The regulation of T-cell trafficking in secondary lymphoid tissues by CCL21 is therefore a tight
131 nductive phase of the immune response in the secondary lymphoid tissues by IL-10-independent mechanis
132 temperatures stimulate lymphocyte homing to secondary lymphoid tissues by increasing L-selectin and
133 bution of infused CD8 T cells, especially in secondary lymphoid tissues, by minimizing ex vivo cultur
134 that circulating CLL cells and those within secondary lymphoid tissues can make AID mRNA and protein
136 to the CC chemokine receptor (CCR)7 ligands secondary lymphoid tissue chemoattractant (SLC) and macr
137 n segments displaying high levels of luminal secondary lymphoid tissue chemokine (SLC) (6Ckine, Exodu
139 e expression of thymic medullary chemokines (secondary lymphoid tissue chemokine (SLC) and EBV-induce
140 pha), thymus-expressed chemokine (TECK), and secondary lymphoid tissue chemokine (SLC) but not of oth
141 cells (DCs) genetically modified to express secondary lymphoid tissue chemokine (SLC) into growing B
147 emotactic responses of LPS-stimulated DCs to secondary lymphoid tissue chemokine (SLC)/CC chemokine l
149 implicated particularly in T-cell movement, secondary lymphoid tissue chemokine (SLC, CCL21) and Eps
150 HEV-decorated homeostatic chemokines such as secondary lymphoid tissue chemokine (SLC; CCL21) to its
151 press CCR7 at high levels and migrate toward secondary lymphoid tissue chemokine and ELC (macrophage-
152 lecules, including the chemotactic molecules secondary lymphoid tissue chemokine and Fas ligand and t
154 transgenic mice with mice expressing CCL21 (secondary lymphoid tissue chemokine) revealed that CCL21
155 of thymus-derived chemotactic agent (TCA)-4 (secondary lymphoid tissue chemokine, 6Ckine, Exodus-2) i
156 n 1, macrophage inflammatory protein 1 beta, secondary lymphoid tissue chemokine, and interleukin 8)
157 immature DC, but not homeostatic chemokines secondary lymphoid tissue chemokine, CCL21, or stromal c
158 and activation-regulated chemokine/CCL17 or secondary lymphoid tissue chemokine/CCL21, caused a 50-7
163 (TARC), C10), and d) constitutive (lungkine, secondary lymphoid-tissue chemokine (SLC), EBI1-ligand c
164 a chemokine represented in the EST database, secondary lymphoid-tissue chemokine (SLC), is expressed
166 6), and regulatory chemokine receptors CCR7 (secondary lymphoid-tissue chemokine (SLC)/CC ligand (CCL
167 ndary lymphoid tissue-associated) chemokines secondary lymphoid-tissue chemokine and macrophage infla
168 ctivation-regulated chemokine) and CCR7 (for secondary lymphoid-tissue chemokine and macrophage infla
169 s, macrophage inflammatory protein 3beta and secondary lymphoid-tissue chemokine significantly (P < 0
170 ogenic signaling pathways, and that--outside secondary lymphoid tissues--clonal evolution is retarded
171 arily reside in nonlymphoid tissues, whereas secondary lymphoid tissues contain functionally quiescen
172 omal derived factor 1 alpha [SDF-1 alpha] or secondary lymphoid tissue cytokine), and ERM proteins lo
174 h congenital defects in different aspects of secondary lymphoid tissue development are beginning to c
175 s, now recognized to be essential for normal secondary lymphoid tissue development, is also a feature
176 xpression of mature DC-specific marker CD83, secondary lymphoid tissue-directing chemokine receptor C
177 a state of dysbiotic hyperimmune response at secondary lymphoid tissues draining local gut and system
178 racrine IL-2 produced in the T cell zones of secondary lymphoid tissues due to their expression of th
179 within CD4(+) T cells in B cell follicles of secondary lymphoid tissues during asymptomatic disease.
180 t T-cell activation and effector function in secondary lymphoid tissues during fungal infection is ch
182 we find expression of H(1gj) in primary and secondary lymphoid tissues early in life, but in adults
183 phocyte trafficking, the BM can supplant the secondary lymphoid tissue either as a site of primary im
184 ntation and the increased APC recruitment to secondary lymphoid tissues expand the scope of known adj
186 y to transport antigen from the periphery to secondary lymphoid tissues for the activation of naive T
187 induced mouse plasmacytomas were detected in secondary lymphoid tissues from normal mice, chiefly in
188 itative imaging in mice to show that, within secondary lymphoid tissues, highly suppressive Treg cell
189 go chemokine receptor switch from CD45RA(+) (secondary lymphoid tissue homing) to CD45RO(+) type (lym
190 expansion of tumor-specific CD8+ T cells in secondary lymphoid tissue; however, CD8+ T cells that ha
191 g Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic
192 key cell players that drive the formation of secondary lymphoid tissue in early human development.
193 tivation and proliferation of lymphocytes in secondary lymphoid tissue in response to infection.
194 XCL9/monokine induced by gamma interferon in secondary lymphoid tissue in SIV infection, no differenc
195 rehensive evaluation of humoral immunity and secondary lymphoid tissues in an established KS (Kmt2d(+
196 en-specific T-cell abundance was observed in secondary lymphoid tissues in either acute or persistent
197 s patches (PPs) are unique compared to other secondary lymphoid tissues in their continual exposure t
198 olved in the development and organization of secondary lymphoid tissues, in the pathogenesis of EAE.
199 ed with B(Mem) frequency differences between secondary lymphoid tissues indicating an influence of lo
200 ted indefinitely in recipient mice that lack secondary lymphoid tissue, indicating that the alloimmun
201 e lymphoid and nonlymphoid components of the secondary lymphoid tissues, information concerning the s
203 ulations of the immune compartment, and that secondary lymphoid tissue is anatomically poised to be r
207 e-directed homing of donor dendritic cell to secondary lymphoid tissues is essential for host sensiti
208 s, the initial accumulation of prions within secondary lymphoid tissues is essential for the transmis
209 Movement of T and B lymphocytes through secondary lymphoid tissues is likely to involve multiple
210 +) Tregs early but not late postinfection in secondary lymphoid tissues is more efficacious in contro
211 The number of B lymphocytes in primary and secondary lymphoid tissues is normal in B7.2 transgenic
214 trate that SPAG6 is expressed in primary and secondary lymphoid tissues, is associated with the centr
215 +) T cells have been identified in different secondary lymphoid tissues, it is not known which subpop
216 ally resident T cells and those that entered secondary lymphoid tissue later were primed in very diff
218 rprisingly, in spite of the severe defect in secondary lymphoid tissue, LTalpha(-/-) mice could clear
221 id tissue induced by TMPD not only resembles secondary lymphoid tissue morphologically, but it also d
223 o homing of DC from peripheral s.c. sites to secondary lymphoid tissue of syngeneic or allogeneic rec
225 type and cytokine patterns in the thymus and secondary lymphoid tissues of FIV-infected cats were inv
228 upregulated in intestinal effector sites and secondary lymphoid tissues of intranasally immunized BAL
232 iTreg generation and function is limited to secondary lymphoid tissue or whether it can occur within
233 s that are specialized to proliferate in the secondary lymphoid tissues or to fight infection at the
234 ese observations can be generalized to other secondary lymphoid tissues or whether virus compartmenta
235 ered to the CD8+ cells during priming within secondary lymphoid tissues, or alternatively is due to t
236 IL-10-producing cells in circulation and in secondary lymphoid tissues, particularly the spleen (80%
237 (CTL) differentiation, whereas CD8 cells in secondary lymphoid tissue proliferated but were not cyto
238 ncing the formation of memory CD8 T cells in secondary lymphoid tissues, rapamycin inhibits the forma
239 r T cells were those that initially targeted secondary lymphoid tissue, rather than tumor sites, as h
240 emory cell reconstitution lags behind a slow secondary lymphoid tissue recovery, with important impli
241 ory preferences of memory cells dictated the secondary lymphoid tissue requirement for the recall res
244 a cells: short-lived ones that appear in the secondary lymphoid tissue shortly after Ag exposure, and
245 d NK-22 cells, was recently described within secondary lymphoid tissue (SLT) as IL-22(-) when resting
246 an natural killer (NK) cell intermediates in secondary lymphoid tissue (SLT), stage 3 CD34(-)CD117(+)
250 identified a progenitor population in human secondary lymphoid tissues (SLTs) that expressed the tra
252 hogen, engulf and traffic foreign antigen to secondary lymphoid tissues, stimulating antigen-specific
255 inusoids of the liver and only 5% migrate to secondary lymphoid tissues such as lymph nodes, Peyer's
257 A was shown to be predominantly expressed in secondary lymphoid tissues, such as lymph node, spleen,
259 en (Ag) in peripheral tissues and migrate to secondary lymphoid tissues, such as lymph nodes (LNs), w
260 and clustering of circulating leukocytes to secondary lymphoid tissues, such as lymph nodes and Peye
262 t and respond to foreign Ag independently of secondary lymphoid tissues supports the existence of non
263 trafficking to, and poor persistence in, the secondary lymphoid tissues targeted by AIDS viruses.
264 etric analyses of CD8+ T cells isolated from secondary lymphoid tissue that revealed a phenotypic pro
265 Although CD4(+) memory T cells reside within secondary lymphoid tissue, the major reservoir of these
266 sence of a functional ER was demonstrated in secondary lymphoid tissues, then ERalpha expression was
267 ting cells, proliferate and differentiate in secondary lymphoid tissues, then traffic to the infected
268 s and facilitates their rapid sequester into secondary lymphoid tissues, thereby regulating the accum
269 ive vaccine should prevent infection of this secondary lymphoid tissue; therefore, the potential of a
270 c lymphoid tissue morphologically resembling secondary lymphoid tissues, though it is unclear whether
272 ells (MBCs) are generated and diversified in secondary lymphoid tissues throughout the organism.
273 h circulating fetal ILC1-like NKPs travel to secondary lymphoid tissues to initiate the formation of
274 esize that IL-2 can mobilize the NK cells of secondary lymphoid tissues to mediate natural killing du
275 in NOD mice do not require the morphology of secondary lymphoid tissues to support their role in dise
276 ve T cells predominantly recirculate through secondary lymphoid tissue until antigen encounter, while
277 ive T cells continuously recirculate between secondary lymphoid tissue via the blood and lymphatic sy
280 at the expansion of antiviral CD8 T cells in secondary lymphoid tissues was IL-2 independent, whereas
281 drug FTY720 leads to trapping of T cells in secondary lymphoid tissues, we evaluated the possibility
282 I+ DC progenitors that migrated to recipient secondary lymphoid tissue were cells that appeared to ha
284 LTi) cells and mouse adult LTi-like cells in secondary lymphoid tissues were found to release IL-22,
285 of HSV-specific antibody-secreting cells in secondary lymphoid tissues were unaffected by depletion
287 HEV are blood vessels normally found in secondary lymphoid tissue where they are specialized for
288 lls (FDCs) reside within germinal centers of secondary lymphoid tissue where they play a critical rol
289 nonmalignant cells within pseudofollicles in secondary lymphoid tissue where tumor cell proliferation
290 the TTSS to rapidly drive respiratory DCs to secondary lymphoid tissues where these APCs stimulate an
291 irculating memory B cells frequently reenter secondary lymphoid tissue, where they receive signals es
292 ady state and after liver transplantation to secondary lymphoid tissues, where the outcome of their i
294 taneously acquired memory-like properties in secondary lymphoid tissues, where tumor antigen level re
295 naive CD4+ T cells from peripheral blood and secondary lymphoid tissues, which declined at rates that
296 rm across both the T cell repertoire and the secondary lymphoid tissues, while (ii) retaining toleran
297 auses atrophy and dysfunction in primary and secondary lymphoid tissues with a corresponding decrease
298 A polymerase, is preferentially expressed in secondary lymphoid tissues with yet unknown physiologica
299 Donor dendritic cells rapidly migrated into secondary lymphoid tissues within 3 h of transplantation
300 sAg) and membrane-associated Ag (mAg) in the secondary lymphoid tissue, yet how the physical form of