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1 sms that give rise to this ectopic, tertiary lymphoid organ.
2 of the overall architecture of that primary lymphoid organ.
3 in alloantibody production within a tertiary lymphoid organ.
4 ncreased with tumor growth but was absent in lymphoid organs.
5 e maintenance of naive T cells in peripheral lymphoid organs.
6 .g., hematopoietic bone marrow and secondary lymphoid organs.
7 tration with increased formation of tertiary lymphoid organs.
8 ocyte glycoprotein (MOG)-specific T cells in lymphoid organs.
9 as well as their potential functions in non-lymphoid organs.
10 pendent of T-cell trafficking from secondary lymphoid organs.
11 gesting increased homing of TFH to secondary lymphoid organs.
12 of T follicular helper cells within tertiary lymphoid organs.
13 aly/aly-spl(-)) mice devoid of all secondary lymphoid organs.
14 ed stromal niche for innate ILC3 in adaptive lymphoid organs.
15 its effects remain unclear, particularly in lymphoid organs.
16 responses both in the ocular lesions and the lymphoid organs.
17 ir proportion declines with age in secondary lymphoid organs.
18 cusing on germinal centers (GC) in secondary lymphoid organs.
19 es of inflammation, but not for migration to lymphoid organs.
20 o HO-1(+/+) donor kidneys, to the peripheral lymphoid organs.
21 velopment failed, and B cells underpopulated lymphoid organs.
22 ene expression was predominantly detected in lymphoid organs.
23 oper trafficking of lymphocytes to secondary lymphoid organs.
24 approximately 20 min) and clearly visualized lymphoid organs.
25 hroughout the intestine but rare in systemic lymphoid organs.
26 eveloped germinal centers (GCs) in secondary lymphoid organs.
27 highly specialized immune cells in secondary lymphoid organs.
28 functional compartmentalization of secondary lymphoid organs.
29 le in the organization of vertebrate mucosal lymphoid organs.
30 lood vessels for lymphocyte extravasation in lymphoid organs.
31 onal germinal center TFH in normal secondary lymphoid organs.
32 an occur in recipient mice lacking secondary lymphoid organs.
33 ndothelium and trafficking through secondary lymphoid organs.
34 human cord blood, BM, blood, and peripheral lymphoid organs.
35 therosclerosis and the formation of tertiary lymphoid organs.
36 ng and compartmentalization within secondary lymphoid organs.
37 for the proper position of B lymphocytes in lymphoid organs.
38 nter reaction in both secondary and tertiary lymphoid organs.
39 take place outside of primary and secondary lymphoid organs.
40 1PR1) is critical for lymphocyte egress from lymphoid organs.
41 reg) with a significant decrease of iTreg in lymphoid organs.
42 ty is initiated in T-cell zones of secondary lymphoid organs.
43 hile preserving their migration to secondary lymphoid organs.
44 ers of T helper 17 (Th17) cells in secondary lymphoid organs.
45 ulatory T cells in the thymus and peripheral lymphoid organs.
46 intricate cellular networks within secondary lymphoid organs.
47 rofound lymphopenia and impaired egress from lymphoid organs.
48 ed early IL-22 production from the liver and lymphoid organs.
49 CXCR3 expression by OT-I cells in secondary lymphoid organs.
50 occurred normally in mice lacking secondary lymphoid organs.
51 cells (APC) into the tumor bed, but not into lymphoid organs.
52 iates the exit of lymphocytes from secondary lymphoid organs.
53 d mature iNKT cells are absent in peripheral lymphoid organs.
54 ammatory Th2 and IL-10 response in secondary lymphoid organs.
55 ologically, however, are the ones present in lymphoid organs.
56 adaptive immune systems and within secondary lymphoid organs.
57 ate and orient immune responses in secondary lymphoid organs.
58 entional and plasmacytoid DC compartments in lymphoid organs.
59 sions targeting mainly the intestine and the lymphoid organs.
60 the development and homeostasis of secondary lymphoid organs.
61 tla4(-/-) T cells to accumulate in secondary lymphoid organs.
62 nct tolerogenic cell population in secondary lymphoid organs.
63 e Peyer's patches but not of other secondary lymphoid organs.
64 totic debris into the follicles of secondary lymphoid organs.
65 D3(+)CD4(+)FOXP3(+) T cells was decreased in lymphoid organs.
66 tream and the trafficking of T cells through lymphoid organs.
67 tory T cells in atherosclerotic arteries and lymphoid organs.
68 een on a majority of CD8(+) TILs, but not in lymphoid organs.
69 gnal was paralleled by CXCR4 upregulation in lymphoid organs.
70 e germinal center (GC) reaction in secondary lymphoid organs.
71 ffective trafficking of PrP(Sc) to secondary lymphoid organs.
72 affected tissue typically develops tertiary lymphoid organs.
73 n of DN T cells in the kidneys and secondary lymphoid organs.
74 (+) B lymphocytes in blood, bone marrow, and lymphoid organs.
75 tical for the egress of T and B cells out of lymphoid organs.
76 ng their recruitment to inflamed tissues and lymphoid organs.
77 ) T cells to the inflamed skin and secondary lymphoid organs.
78 iently trigger immune responses in secondary lymphoid organs.
79 within atherosclerotic lesions or secondary lymphoid organs.
80 cell frequency in the thymus and peripheral lymphoid organs.
81 8(+) DP cells in peripheral lymphoid and non-lymphoid organs.
82 ile excessive IL-22 induced atrophy in these lymphoid organs.
83 cterized by contracted populations homing to lymphoid organs.
84 , most cellular immune interactions occur in lymphoid organs.
85 ic role for stromal cell niches in secondary lymphoid organs after allo-BMT and define a framework of
86 egs (pTregs) that are generated in secondary lymphoid organs after exposure to antigen and specific c
88 the plasma membrane; however, their fate in lymphoid organs after their release remains controversia
90 we take advantage of tractable primary human lymphoid organ aggregate cultures to show that IL-21 dir
91 ent studies on human TFH cells isolated from lymphoid organ and blood samples and recent observations
93 ession of IL-22 and its receptor (IL-22R) in lymphoid organ and target tissues was determined during
95 , designed to enhance targeting of secondary lymphoid organs and activation of APCs, have shown subst
96 trafficking and migration through secondary lymphoid organs and at peripheral infection sites, highl
100 ed as continuously recirculating through the lymphoid organs and blood, lymphocytes also establish re
102 sts prevent lymphocyte egress from secondary lymphoid organs and cause a reduction in the number of c
103 and the regulation of S1P gradients between lymphoid organs and circulatory fluids in homeostasis ar
105 ith a decreased noradrenergic innervation of lymphoid organs and counteracted the immunosuppressive e
108 he initially robust GC response in secondary lymphoid organs and exhibit reduced antiviral serum IgG
109 ltaARE mice also present mesenteric tertiary lymphoid organs and have altered lymphatic transport of
110 in trafficking of naive T cells to secondary lymphoid organs and in Ag-dependent T cell activation in
111 understanding of how various DC subsets, in lymphoid organs and in the periphery, can be targeted th
112 ocated from the small intestine to secondary lymphoid organs and increased the intratumoral CD8/Treg
113 es or to temporal niches present in reactive lymphoid organs and inflamed tissues, structures where T
115 1-deficient T cells home less efficiently to lymphoid organs and migrate more slowly through them.
118 2 and IL-33 increased the number of Tregs in lymphoid organs and protected mice from ischemia-reperfu
119 ed mouse cell populations were isolated from lymphoid organs and purified by multiparameter fluoresce
120 mmune response involves T-cell activation in lymphoid organs and subsequent migration to peripheral t
121 ly regulated the egress of Treg cells out of lymphoid organs and subsequent non-lymphoid tissue distr
122 markedly improve Ag/adjuvant co-delivery to lymphoid organs and sustain Ag presentation on dendritic
123 their localization, as TCM home to secondary lymphoid organs and TEM circulate through non-lymphoid t
124 antigens may be organized by artery tertiary lymphoid organs and that disruption of the balance betwe
125 tary retinoids control the size of secondary lymphoid organs and the efficiency of immune responses i
126 ologic memory, yet their distribution within lymphoid organs and the individual role of these for mBC
127 timulated dendritic cells (DCs) to secondary lymphoid organs and their interaction with Ag-specific T
128 lls persisted as central memory cells in the lymphoid organs and tissue-resident memory cells in the
130 whether IL-27 is produced by human secondary lymphoid organs and what is its functional role on human
131 ratory mouse strains ( approximately 0.1% in lymphoid organs), and lack of an appropriate mouse model
132 primary purview of Tregs circulating through lymphoid organs, and homeostasis ensured mainly by their
133 accumulation of migratory dendritic cells in lymphoid organs, and increased Th1 immune responses in v
134 ritical for lymphocyte egress from secondary lymphoid organs, and S1P receptor modulators suppress ly
135 nalysis of donor T cells in blood, secondary lymphoid organs, and target organs of aGvHD after BMT sh
136 S1P is higher in circulatory fluids than in lymphoid organs, and the S1P1 receptor (S1P1R) directs t
137 n proximity to germinal centers in secondary lymphoid organs, and their memory compartment also circu
138 organized similar to follicles in secondary lymphoid organs, and we provide inferential evidence for
140 at circulate in the blood and are present in lymphoid organs are an essential component of long-lived
142 autonomic nervous system and immune cells in lymphoid organs are known to contribute to systemic immu
143 typically naive Tr cells occupying secondary lymphoid organs are largely supported by paracrine IL-2
144 oing anti-HBV CD8(+) T cell responses in the lymphoid organs are largely unknown due to the infeasibi
145 tion of the inhibitory noradrenergic tone in lymphoid organs as one of the possible explanations for
147 he migration dynamics of immune cells within lymphoid organs at the steady state and on how these dyn
148 hough VSMC-LTbetaRs did not affect secondary lymphoid organs: Atherosclerosis was markedly exacerbate
149 d mice is due to Treg expansion in secondary lymphoid organs because depletion of Tregs restored humo
150 the bloodstream and proliferate in secondary lymphoid organs before replenishing effector and memory
151 n vivo-generated PCs isolated from secondary lymphoid organs, blood (circulating, recently Ag-induced
153 controlling macrophage function not only in lymphoid organs but also in end organs, thereby preventi
154 Mantle cell lymphoma (MCL) accumulates in lymphoid organs, but disseminates early on in extranodal
155 tes of parasite replication and in secondary lymphoid organs, but the factors that regulate this expa
156 ACs) have been described in murine secondary lymphoid organs, but the identity of such cells and thei
157 fective development of B cells and secondary lymphoid organs, but the role of NIK in adult animals ha
158 ction as a homeostatic cytokine in secondary lymphoid organs by limiting duration and/or intensity of
160 lecules, and impeded Treg cell homing to non-lymphoid organs, causing CD8(+) T-cell-mediated autoimmu
161 rong migratory capacity toward the secondary lymphoid organ chemokine CCL21 and retained a functional
164 blocking co-inhibitory signals in secondary lymphoid organs, cytotoxic T-lymphocyte antigen (CTLA)-4
165 reduced numbers of T cells in the peripheral lymphoid organs, developed significantly less tumors com
166 tudied for its function in the regulation of lymphoid organ development and B-cell maturation, the ro
167 organization, immune response, hematopoietic/lymphoid organ development, and myeloid/leukocyte differ
169 of activated B cells that form in secondary lymphoid organs during a T-dependent immune response.
170 ral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent viral infect
173 apid but reversible disruption of intestinal lymphoid organs during systemic viral immune activation.
175 re more resistant to apoptosis than those in lymphoid organs during the resolution and memory phase o
176 issues (NALTs), which are mucosal-associated lymphoid organs embedded in the submucosa of the nasal p
179 t is maintained after migration to secondary lymphoid organs, favors preferential induction of antige
181 Intestinal Peyer's patches are essential lymphoid organs for the generation of T cell-dependent i
182 ression of chemokines required for secondary lymphoid organ formation and thus plays a pivotal role i
185 ions, allowing visualization of intact mouse lymphoid organs from a collection of immunolabeled slice
188 VHD model enabled visualization of secondary lymphoid organs harboring activated donor T cells prior
190 ive Foxo1 mutant prevented downregulation of lymphoid organ homing molecules, and impeded Treg cell h
192 ens trafficking of T cells through secondary lymphoid organs, impairs the infiltration of T cells int
193 preferentially colonizes Peyer's patches, a lymphoid organ in which microfold cells (M cells) overla
194 s of FOXP3(+) T cells in blood and secondary lymphoid organs in 2D2 MOG-specific transgenic mice, and
195 phoid follicles (LFs), which may function as lymphoid organs in chronic obstructive pulmonary disease
196 H2-DM genes on parasite dissemination toward lymphoid organs in mice, as well as activation of CD4(+)
197 ecent research characterized artery tertiary lymphoid organs in the aorta adventitia of aged apolipop
198 led to the increased development of tertiary lymphoid organs in the aorta, and enhanced disease devel
199 ell activation is normally restricted to the lymphoid organs, in part because of their limited abilit
200 P) guides T cell circulation among secondary lymphoid organs, including spleen, lymph nodes and Peyer
202 1P) mediates egress of immune cells from the lymphoid organs into the lymphatic vessels; we investiga
203 ition within primary, secondary, or tertiary lymphoid organs is a prerequisite to ensure immune cells
204 at the increased proportion of DN T cells in lymphoid organs is associated with a decrease in both di
206 enting cells with T lymphocytes in secondary lymphoid organs is essential for the initiation of alloi
208 in overactivation of this axis in secondary lymphoid organs, led to the increased development of ter
212 r, neither T cell recruitment into secondary lymphoid organs nor initial T cell activation was affect
215 hat MKP-2 mRNA levels in the spinal cord and lymphoid organs of EAE mice were increased compared with
217 mined that functional human ILC3s develop in lymphoid organs of humanized mice and that persistent HI
218 Through the analysis of GFP expression in lymphoid organs of IL-21eGFP mice, we identified a subpo
219 ells of the TH17 subset of helper T cells in lymphoid organs of naive mice 'preferentially' homed to
220 donor passenger leukocytes to the secondary lymphoid organs of the recipient to elicit an immune res
221 SC accumulation in bone marrow and secondary lymphoid organs of tumor-bearing hosts remain unclear.
222 ory T cell compartment present in peripheral lymphoid organs of unmanipulated mice expresses Il23r ex
223 , we noted an increase in SD-4(+) T cells in lymphoid organs of wild-type (WT) mice immunized for EAE
224 e structures (ELSs) reminiscent of secondary lymphoid organs often develop at sites of chronic inflam
225 Although proliferation remains located in lymphoid organs only, suggesting a major role of the tum
227 ase of the intestinal tract, report tertiary lymphoid organs present within the mucosal wall, along w
229 ive T cells that circulate through secondary lymphoid organs ready to be activated upon pathogenic ch
233 ties and differences between mouse and human lymphoid organ-resident TFH cells and discuss the role o
234 ease and subsequent maintenance of secondary lymphoid organ-resident Tr cells are still poorly unders
245 nfected distinct CD4(+) T cells in secondary lymphoid organs (SLOs) and within the lamina propria of
246 of the pathogen and the underlying secondary lymphoid organs (SLOs) needs to be established to prime
248 cribed to circulate between blood, secondary lymphoid organs (SLOs), and lymph in the steady state.
250 d to decreased T-cell migration to secondary lymphoid organs (SLOs), reduced in vivo proliferation wi
251 e progression of autoreactivity in secondary lymphoid organs (SLOs), we characterized the localizatio
255 approximately 25% of mice lacking secondary lymphoid organs spontaneously develop specific antinucle
256 ting immune sentinels that convey signals to lymphoid organ stroma and thereby facilitate immune resp
257 ssing dendritic cells migrate into secondary lymphoid organs, such as lymph nodes, that drain the upp
258 and/or cysteine depletion, was found in the lymphoid organs, such as the spleen and lymph nodes.
259 th characteristics reminiscent of a tertiary lymphoid organ, suggesting the creation of a microenviro
260 s are localized in T cell zones of secondary lymphoid organs, suppress activation and expansion of CD
261 demonstrate that distinct niches within the lymphoid organ T zone support distinct cell fate decisio
262 V-HNSCC) originate in the tonsils, the major lymphoid organ that orchestrates immunity to oral infect
263 nce and function of the immune system and on lymphoid organs that coordinate both the maintenance of
264 gp38(+) fibroblasts, which resemble tertiary lymphoid organs that develop in models of chronic inflam
265 circulate through PB and reside in different lymphoid organs that do not reflect different mBC maturi
267 tion of Peyer's patches (PP), gut-associated lymphoid organs that have a key role in the initiation o
268 d as the main T-cell subset within secondary lymphoid organs that promotes B-cell differentiation lea
270 ific B cells arrive in Ag-draining secondary lymphoid organs, they may join the ongoing GC response.
272 ting adaptive immune responses in peripheral lymphoid organ tissues, how DCs infiltrate the CNS and c
273 The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs followi
276 , B-cell-rich aggregates resembling tertiary lymphoid organs (TLOs) impinged on lymphatic collecting
278 ing Treg (rTreg) cell phenotype in secondary lymphoid organs, Treg cells in non-lymphoid tissues exhi
279 he germinal center, which forms in secondary lymphoid organs upon exposure to antigenic stimuli.
280 epertoire encoded by B cells in the blood or lymphoid organs using high-throughput DNA sequencing tec
286 Because NIK-deficient mice lack secondary lymphoid organs, we generated transgenic mice with targe
287 l conditions within discrete nonlymphoid and lymphoid organs, we show that IL-10 production by CD4(+)
288 (pos)CD127(neg)FoxP3(pos) Tregs in secondary lymphoid organs were proliferating activated CD69(pos)CD
289 the effector/memory phenotype in peripheral lymphoid organs when compared with Cd4[Cre] mice express
290 ess as recent thymic emigrants to peripheral lymphoid organs where they undergo an additional maturat
291 s) are known to inhabit T cell-rich areas of lymphoid organs, where they function to facilitate inter
292 /-) mice showed a global reduction of DCs in lymphoid organs, whereas development of granulocytes and
293 e back and forth between blood and secondary lymphoid organs, whereas in the second, memory cells rec
294 eg cell numbers in the thymus and peripheral lymphoid organs, whereas it did not alter conventional C
295 activated by self-draining OVA+CAF09 in the lymphoid organs, whereas the CD103(+) DCs are stimulated
296 T cells proved hyporesponsive in peripheral lymphoid organs, whereas they retained effector function
297 We propose that the restriction of oxygen in lymphoid organs, which can be altered in pathophysiologi
298 self-drainage of the adjuvant/antigen to the lymphoid organs, which takes place upon i.p. immunizatio
299 ase of immune cell infiltration in secondary lymphoid organs with a marked effect on the presence of
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