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1 to neurotransmission, vasoconstriction, and lymphocyte proliferation.
2 ive oxygen intermediates, which can suppress lymphocyte proliferation.
3 a potential mechanism by which HTLV-1 alters lymphocyte proliferation.
4 n kinase A as potential targets for altering lymphocyte proliferation.
5 ine the mechanism by which CO can modulate T lymphocyte proliferation.
6 (Z-VAD-FMK pan-caspase inhibitor) blocked T lymphocyte proliferation.
7 , IL-2, IL-4, IL-5, and IL-10 production and lymphocyte proliferation.
8 mulatory molecules required for AChR-induced lymphocyte proliferation.
9 L-2 receptors and thus is a key regulator of lymphocyte proliferation.
10 the coccidioidal Ag preparation T27K induced lymphocyte proliferation.
11 t activate NF-kappaB and did not stimulate B lymphocyte proliferation.
12 mino acids that are known to be required for lymphocyte proliferation.
13 coimmobilized with anti-CD3 mAb, activated T lymphocyte proliferation.
14 lity of 11 L-tryptophan analogues to support lymphocyte proliferation.
15 e [DP]) cells, and antigen-specific mature T-lymphocyte proliferation.
16 ation promotes continued TCR signaling and T-lymphocyte proliferation.
17 ocess the appropriate Ags for stimulation of lymphocyte proliferation.
18 ction of PBMC responses to peptides than did lymphocyte proliferation.
19 negatively, respectively, with inhibition of lymphocyte proliferation.
20 roduction alone is not sufficient to inhibit lymphocyte proliferation.
21 ability to inhibit lymphokine production and lymphocyte proliferation.
22 osis factor (TNF) family that costimulates B lymphocyte proliferation.
23 circulating carotenoid concentrations and T lymphocyte proliferation.
24 f the immune system, leading to increases in lymphocyte proliferation.
25 ly cytokine production, HLA expression, or T lymphocyte proliferation.
26 mplex with apalbumin1 capable of stimulating lymphocyte proliferation.
27 volve inhibition of T cell activation and/or lymphocyte proliferation.
28 of IL-2, IFN-gamma, and TNF-alpha, and on T lymphocyte proliferation.
29 However, Fas engagement also can costimulate lymphocyte proliferation.
30 ssessed by delayed type hypersensitivity and lymphocyte proliferation.
31 rom ConA-stimulated T lymphocytes enhanced B-lymphocyte proliferation.
32 e drug rapamycin inhibits cytokine-dependent lymphocyte proliferation.
33 4 replicated this differential modulation of lymphocyte proliferation.
34 + cells functionally suppressed autologous T-lymphocyte proliferation.
35 on of FoxO in the nucleus and attenuation of lymphocyte proliferation.
36 ed that surfactant protein A (SP-A) inhibits lymphocyte proliferation.
37 er was combined with anti-caCD3 to stimulate lymphocyte proliferation.
38 nditional deletion of FADD leads to impaired lymphocyte proliferation.
39 nflagration associated with infection-driven lymphocyte proliferation.
40 nt to participate in cytokine production and lymphocyte proliferation.
41 blockade also reduced alloantigen-specific T lymphocyte proliferation.
42 an inflammatory ocular disease by inhibiting lymphocyte proliferation.
43 yte apoptosis, is paradoxically required for lymphocyte proliferation.
44 gulatory T cell recruitment and control of T lymphocyte proliferation.
45 neutralization of MIG/CXCL9 in MLR reduced T lymphocyte proliferation, 4) IFN-gamma-inducible protein
46 moattractant/CXCL11 had similar effects on T lymphocyte proliferation, 5) MIG/CXCL9 stimulated T lymp
47 blood cells were associated with impaired T lymphocyte proliferation, abnormal mononuclear cell cyto
51 imals with each protein and assaying splenic lymphocyte proliferation against a series of overlapping
53 elated with inhibition of mitogen-stimulated lymphocyte proliferation, although urease inhibited IL-2
65 ell production but does increase CD4 and CD8 lymphocyte proliferation and death by inducing entry int
68 een Myc and Mad levels may normally modulate lymphocyte proliferation and development in part by cont
70 tudies showed that D-4F reduced allogeneic T-lymphocyte proliferation and effector cytokine productio
71 udy demonstrates that MIG/CXCL9 stimulates T lymphocyte proliferation and effector cytokine productio
72 asal route showed increased antigen specific lymphocyte proliferation and enhanced the frequency of T
73 and NFATs (NFATc and NFATp), and c) inhibits lymphocyte proliferation and expression of proinflammato
75 and bacterioferritin as measured by splenic lymphocyte proliferation and gamma interferon production
77 unoglobulin G2 (IgG2) and stimulate memory T-lymphocyte proliferation and gamma interferon secretion.
81 stimulation assays revealed no difference in lymphocyte proliferation and IL-2 secretion between EGFP
83 ion of lymph nodes, H(4)R antagonism reduced lymphocyte proliferation and IL-4, IL-5, and IL-17 level
84 ession, IL-2- enhanced IFN-gamma production, lymphocyte proliferation and immune cell phenotype analy
85 eloid lineage and to selectively stimulate B-lymphocyte proliferation and immunoglobulin production.
86 B/WcKO mice, B/DcKO mice showed defective B-lymphocyte proliferation and impaired antibody responses
87 ia coli and all three parasites stimulated B-lymphocyte proliferation and increased macrophage produc
88 endrobatidis cells and supernatants impaired lymphocyte proliferation and induced apoptosis; however,
89 ultures, allogeneic CDCs elicited negligible lymphocyte proliferation and inflammatory cytokine secre
90 were induced after treatment, as measured by lymphocyte proliferation and interferon gamma enzyme-lin
92 t encodes a toxin that specifically inhibits lymphocyte proliferation and interleukin-2 (IL-2), IL-4,
94 Mycophenolic acid (MPA) is an inhibitor of lymphocyte proliferation and is well established as an i
97 In vitro assays showed correction of the lymphocyte proliferation and neutrophil adhesion defects
98 between healthy eating patterns and greater lymphocyte proliferation and no evidence for an associat
99 of folate-deficient cells rapidly restored T lymphocyte proliferation and normal cell cycle, reduced
100 TAK-779 (a) decreased alloantigen-specific T-lymphocyte proliferation and number of IFN-gamma produci
101 the importance of metabolism in controlling lymphocyte proliferation and offer a novel explanation f
102 ith T lymphocytes and macrophages to cause T lymphocyte proliferation and overwhelming cytokine produ
105 synthesized and evaluated for inhibition of lymphocyte proliferation and production of pro-inflammat
106 of transforming growth factor type beta1 on lymphocyte proliferation and production of tumor necrosi
107 ic E. coli (lifA) mediates the inhibition of lymphocyte proliferation and proinflammatory cytokine sy
108 ermined that iPSC-MSCs significantly inhibit lymphocyte proliferation and promote Treg response in PB
109 1 has an essential role in mediating B and T lymphocyte proliferation and requires its CARD to engage
113 itantly, they up-regulated genes involved in lymphocyte proliferation and survival, most notably inte
116 ne being able to functionally promote both T lymphocyte proliferation and T(H)1 cytokine production.
117 H/HeJ mice were less potent stimulators of T lymphocyte proliferation and TH1/TH17 polarization compa
118 cellular responses, as measured by in vitro lymphocyte proliferation and Th2 cytokine production (i.
119 ization of CXCR3 reduced MIG/CXCL9-induced T lymphocyte proliferation and the number of IFN-gamma-pos
121 dy was to determine whether CO can inhibit T lymphocyte proliferation and then to determine the mecha
123 that colon tumors expressing LIGHT stimulate lymphocyte proliferation and tumor cell-specific antitum
126 oid and natural killer cell numbers, reduced lymphocyte proliferation, and abrogated phagocyte activi
127 sate (TSL), induce DC maturation, autologous lymphocyte proliferation, and antigen-specific lymphocyt
129 ponses (delayed-type hypersensitivity [DTH], lymphocyte proliferation, and cytokine production) were
130 n peripheral blood leukocyte subpopulations, lymphocyte proliferation, and cytokine responses were me
131 on with either tacrolimus or cyclosporine on lymphocyte proliferation, and expression of interleulin-
132 -1-specific immunoglobulin G (IgG) titers, T-lymphocyte proliferation, and gamma interferon productio
133 serologic responses to Salmonella Typhi LPS, lymphocyte proliferation, and interferon (IFN)- gamma pr
134 vitreous infiltrates, fewer granulomas, less lymphocyte proliferation, and lower serum IRBP antibody
135 rmation and proinflammatory cytokine levels, lymphocyte proliferation, and neutrophil recruitment.
136 resulted in lactate accumulation, inhibited lymphocyte proliferation, and prevented immunoglobulin p
138 f clonal selection requires a rapid burst in lymphocyte proliferation, and this involves a metabolic
139 immunosuppression by its ability to inhibit lymphocyte proliferation, and with neurotoxicity through
140 sing inhibition of BLV-dependent spontaneous lymphocyte proliferation as a measure of antiviral activ
142 7 treatment resulted in potent inhibition of lymphocyte proliferation as measured by in vitro mitogen
143 nt Ags 85A, 85B, and 85C induced significant lymphocyte proliferation as well as the production of ga
144 The 35-kDa protein also induced significant lymphocyte proliferation as well as the production of IF
145 dex showed modest effects of Myc to increase lymphocyte proliferation, as normal lymphocytes already
146 The early response was characterized by T-lymphocyte proliferation, as reflected by S-phase DNA, w
147 ed baseline interferon gamma (IFN-gamma) and lymphocyte proliferation assay (LPA) responses to antige
149 PBMC using the dexamethasone suppression of lymphocyte proliferation assay and repeated after the ad
150 ied by enzyme-linked immunosorbent assay and lymphocyte proliferation assay, showing that TprK is the
155 ion of donor-specific reactivity by means of lymphocyte proliferation assays has also been used; howe
156 development was followed by flow cytometry, lymphocyte proliferation assays, and T-cell receptor Vbe
160 munodeficiency virus type 1 (HIV-1)-specific lymphocyte proliferation before and after treatment with
161 phorylation and impaired IL-4-induced CD4+ T lymphocyte proliferation but left unperturbed Stat6 acti
162 has been widely applied to investigate human lymphocyte proliferation, but solid tissue samples may a
163 nal transduction pathways regulating B and T lymphocyte proliferation, but the functional role of Ca(
164 Its most prominent mechanism is to inhibit lymphocyte proliferation by inhibition of inosine monoph
165 cted children and suggest that inhibition of lymphocyte proliferation by MV may play a role in the su
166 This study demonstrates that inhibition of lymphocyte proliferation by nonpolymorphic MHC class II
167 onducted to measure chemokine production and lymphocyte proliferation by peripheral blood mononuclear
168 trate that hydroquinone and catechol inhibit lymphocyte proliferation by quenching the essential tyro
171 ne exchange factors plays a critical role in lymphocyte proliferation, cytoskeletal reorganization, a
172 tion of toleragenic cytokines, inhibition of lymphocyte proliferation, delivery of reparative and pro
174 l-mediated inhibition of anti-CD3-stimulated lymphocyte proliferation did not require cell contact.
175 immune signals and metabolic cues to direct lymphocyte proliferation, differentiation and survival.
176 g the effect of adipocytes and adipokines on lymphocyte proliferation, differentiation, and activatio
177 e involved in signaling cascades mediating T-lymphocyte proliferation, differentiation, and migration
178 to maintain tolerance via the regulation of lymphocyte proliferation, differentiation, and survival.
179 ored, IFN-inducible protein that regulates T lymphocytes proliferation, differentiation, and developm
180 here is a paucity of data demonstrating that lymphocyte proliferation does occur in humans treated wi
181 3-kinase (PI3K) activation is essential for lymphocyte proliferation driven by receptors for antigen
184 calcineurin (eg, cyclosporine, tacrolimus), lymphocyte proliferation (eg, azathioprine, mycophenolat
186 feration following partial hepatectomy and T lymphocyte proliferation following anti-CD3 stimulation
187 h1 immune response characterized by in vitro lymphocyte proliferation, gamma interferon production, a
189 demonstrate the importance of this factor in lymphocyte proliferation, gene expression, and Th cell d
190 However, both methods necessitate in vitro lymphocyte proliferation, generating highly differentiat
193 lymphocyte functionality (CD4(+) and CD8(+) lymphocyte proliferations, IFN-gamma production, STAT5 p
194 or cyclosporine significantly inhibited the lymphocyte proliferation, IL-2 expression, and induced T
196 arried out a prospective kinetic analysis of lymphocyte proliferation in 13 rhesus macaques inoculate
198 Finally, DC stimulated Candida-specific lymphocyte proliferation in a concentration-dependent ma
199 d that 1) exogenous MIG/CXCL9 stimulated CD4 lymphocyte proliferation in a MHC class II-mismatched ML
201 ished the capacity of these moDC to induce T lymphocyte proliferation in both autologous and allogene
202 immune-induced wasting and enhanced ex vivo lymphocyte proliferation in broilers and decreased tumor
203 ls as detected by intracellular staining and lymphocyte proliferation in culture after BeSO(4) exposu
204 yte proliferation, 5) MIG/CXCL9 stimulated T lymphocyte proliferation in MHC class I- and total MHC-m
206 osome-depleted, nonpromoter sites to drive B-lymphocyte proliferation in primary human infection.
207 al loads in the presence of both antibodies, lymphocyte proliferation in response to blood monocytes
209 cellular immunity, characterized by reduced lymphocyte proliferation in response to both parasite an
210 II expression in the reproductive tract and lymphocyte proliferation in response to mitogenic and ch
212 us studies showed that SP-A and SP-D inhibit lymphocyte proliferation in the presence of accessory ce
213 bserve gene expression changes indicative of lymphocyte proliferation in the spleen, which is associa
214 PX3.102 markedly suppressed antigen-specific lymphocyte proliferation in vitro at a concentration 10
219 tudinal analyses of neutralizing antibodies, lymphocyte proliferation, in vivo-activated and memory c
221 ns, specifically suppressed peripheral blood lymphocyte proliferation, induced expression of a wide p
223 elayed-type hypersensitivity, enhancement of lymphocyte proliferation, induction of an innate IL-12 r
226 Although PI3K activation is required for B-lymphocyte proliferation, it is not known whether PI3K-d
230 This peptide was more bioactive against lymphocyte proliferation, nearly equivalent to the comme
233 cells, and they show an inhibitory effect on lymphocyte proliferation of two LST1 proteins although t
237 F-alpha; however, we measured no change in T lymphocyte proliferation or in the percentage of alveola
238 were failure to demonstrate either impaired lymphocyte proliferation or maternal T-cell engraftment.
239 significantly affect antigen-specific recall lymphocyte proliferation or type 1 cytokine production i
240 an autoantigen for IPF CD4 T cells, inducing lymphocyte proliferation (P = 0.004) and IL-4 production
241 tion of cytokine responses in the absence of lymphocyte proliferation, particularly during the early
242 pport emerging evidence that HTLV-1 promotes lymphocyte proliferation preceding early viral spread in
243 , there is a significant discrepancy between lymphocyte proliferation rates estimated in different st
244 IgG subclass deficiency, impaired Ag-induced lymphocyte proliferation, reduced cytokine production by
246 The presence of chlamydial antibodies and SF lymphocyte proliferation responses were determined in pa
249 BLV viremia was assessed by spontaneous lymphocyte proliferation (SLP) in cultures of blood mono
252 ic immune abnormalities, such as spontaneous lymphocyte proliferation (SP), increased STAT5 phosphory
253 ound that incubator oxygen levels influenced lymphocyte proliferation stimulated by two commonly used
254 and inflammatory responses and contribute to lymphocyte proliferation, survival, and oncogenesis.
255 ne interleukin-7 (IL-7) functions to enhance lymphocyte proliferation, survival, and recruitment of i
256 Cs and bone marrow-derived MSCs (BM-MSCs) on lymphocyte proliferation, T-cell phenotypes and cytokine
262 and diminished microfilarial antigen-driven lymphocyte proliferation than cells from children of uni
263 ess IFN-gamma and TNF-alpha production and T lymphocyte proliferation than in cultures with platelets
264 pleens of acceptors more potently suppressed lymphocyte proliferation than Treg from rejectors in the
265 a potent and selective inhibitor of B and T lymphocyte proliferation that has proven effective in re
266 ment, it was found that the PRRSV-specific T lymphocyte proliferation, the percentages of CD4(+), CD8
267 emonstrate that c-FLIP(L) is essential for T lymphocyte proliferation through an NF-kappaB-independen
268 ABCG1 as an important negative regulator of lymphocyte proliferation through the maintenance of cell
269 gamma-induced intracellular enzyme, inhibits lymphocyte proliferation through tryptophan degradation.
270 ersistent, maximal cytokine production and T lymphocyte proliferation, thus contributing to the devel
274 his study supports the concept that in vitro lymphocyte proliferation to HIV-1 antigens, augmented af
276 ponses to presentation 1 and presentation 2; lymphocyte proliferation to Salmonella Typhi flagellin o
278 ction of virus capsid-specific antibodies or lymphocyte proliferation to the virus antigen (class II
279 n A-stimulated whole blood assays to measure lymphocyte proliferation (tritium labeled thymidine inco
280 a cell cycle inhibitory checkpoint, allowing lymphocyte proliferation, tumor targeting, and regressio
281 udies provide clear evidence that control of lymphocyte proliferation via c-Rel is linked to a cyclin
283 hasone to inhibit phytohemagglutinin-induced lymphocyte proliferation was assessed by (3)H-thymidine
286 d only 10 to 20% by MV coinfection; however, lymphocyte proliferation was decreased by 60 to 90% and
287 and plasma of infected subjects to suppress lymphocyte proliferation was demonstrated by (3)H thymid
288 We found that CD4+CD45RO+ and CD8+CD45RO+ T lymphocyte proliferation was elevated in HTLV-1-infected
289 cultures of PBMCs with iPSC-MSCs or BM-MSCs, lymphocyte proliferation was evaluated using 3H-thymidin
290 al CD8+ T lymphocyte numbers were higher and lymphocyte proliferation was increased in tumor-bearing
293 of 250 parts per million CO, CD3-activated T lymphocyte proliferation was, remarkably, inhibited by 8
294 when hepatocytes were co-cultured with liver lymphocytes, proliferation was inhibited by IFN-gamma/ST
295 To establish the role of c-FLIP(L) in T lymphocyte proliferation, we have generated a conditiona
296 on of glutamate and in the immune system for lymphocyte proliferation, we tested the effect of the gl
297 itreous infiltrates, retinal granulomas, and lymphocyte proliferation were assessed in OPN-null and W
299 n of CD4 lymphocytes significantly decreased lymphocyte proliferation whereas CD8 cell depletion did
300 ctivated dendritic cells induced increased T lymphocyte proliferation within the aorta 72 h after ado
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