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1 lation stimulated by these Dsg3 peptides was CD4 positive.
2       One-third of infiltrating T cells were CD4 positive.
3 ase-line percentage of lymphocytes that were CD4-positive, a higher weight for age, a higher height f
4 ry infiltrate, cluster of differentiation 4 (CD4)-positive and CD8(+) T-lymphocyte levels, and viral
5  activation of cluster of differentiation 4 (CD4)-positive and cluster of differentiation 8 (CD8)-pos
6 tudying the entry of three SIV isolates into CD4-positive and CD4-negative cells expressing different
7                                         Both CD4-positive and CD4-negative peripheral blood dendritic
8 ytes, Kupffer cells, hepatic stellate cells, CD4-positive and CD8-positive lymphocytes, and cholangio
9 culum spp levels were associated with higher CD4-positive and CD8-positive TIL counts.
10  only one, MF275, inhibited the infection of CD4-positive CCR5-positive cells by some HIV-1 strains.
11 e, CCR5-positive cells, but the infection of CD4-positive, CCR5-positive cells was inhibited.
12                          Virus bound to both CD4-positive (CD4(+)) and CD4-negative (CD4(-)) cells, i
13 V challenge, further eliciting robust memory CD4-positive (CD4(+)) and CD8(+) T-cell and ZIKV-specifi
14 tional ability to stimulate antigen-specific CD4-positive (CD4(+)) and CD8(+) T-cell responses.
15 -gp41 heterodimers mediates virus entry into CD4-positive (CD4(+)) cells.
16                                              CD4-positive (CD4(+)) T cells are the main contributors
17 phoid tissues and of IL-4-producing Th2-type CD4-positive (CD4(+)) T cells than did controls.
18                          OVA-specific Ab and CD4-positive (CD4(+)) T-cell responses were determined.
19                                              CD4-positive (CD4+) T cells isolated from mucosal compar
20               Our laboratory discovered that CD4-positive (CD4+) T cells of the immune system convey
21 s mucosal adjuvant requires IL-4 and induces CD4-positive (CD4+) Th2-type responses, while nLT up-reg
22  of PSCA-vaccinated mice were infiltrated by CD4-positive, CD8-positive, CD11b-positive, and CD11c-po
23  infection of a CD4-positive precursor cell (CD4 positive/CD8 positive) with subsequent differentiati
24 B) was defined similarly, using the dates of CD4-positive cell counts or HIV-1 RNA measurements.
25 e of T-tropic HIV viruses is associated with CD4-positive cell decline and progression to AIDS, sugge
26 n immunodeficiency virus-type 1 (HIV-1) on a CD4-positive cell line expressing CCR3 and to a lesser e
27 eath related to HIV-1 infection of the human CD4-positive cell line H9, requires an ICE-like protease
28 hich this antibody blocks HIV-1 entry into a CD4-positive cell.
29 wly and inefficiently adsorbed onto cultured CD4-positive cells at 37 degrees C, and the gradual decl
30                                 Infection of CD4-positive cells by human immunodeficiency virus type
31   To determine whether specific infection of CD4-positive cells could be demonstrated for these recom
32                Finally, adoptive transfer of CD4-positive cells from GF, but not SPF mice induces sev
33  organs, and in the presentation of virus to CD4-positive cells in multiple locations including lymph
34 HIV-1 is able to infect cultured susceptible CD4-positive cells in standard assay conditions casts do
35 ayed increased numbers of CD25-, FoxP3-, and CD4-positive cells in the CNS.
36 s, there was almost a complete lack of naive CD4-positive cells in the control tumors, a situation th
37 ulovirus powerfully induces proliferation of CD4-positive cells originating from several different sp
38 line produces virions capable of transducing CD4-positive cells with high efficiency (up to 10(5) cel
39                          Extensive fusion of CD4-positive cells with the chimeric protein containing
40                                              CD4-positive cells with TRIM33 knock down show increased
41 lecules were found on the plasma membrane in CD4-positive cells, 43.9 +/- 8.5% were found in CD4-nega
42 e, psi 422, psi 422 cells form syncytia with CD4-positive cells, correctly express HIV-1 structural p
43 nes in stimulating HIV-1 replication in high CD4-positive cells, including primary lymphocytes, but n
44 nalization of CXCR4 in both CD4-negative and CD4-positive cells, suggesting that gp120 is a high affi
45 ated cell-cell fusion and virus infection of CD4-positive cells.
46 kine receptors CCR5 and CXCR4 for entry into CD4-positive cells.
47 ins and can transmit bound virus to adjacent CD4-positive cells.
48 Env cells only upon exposure to soluble CD4, CD4-positive, coreceptor-negative cells, or stromal cell
49             In single-round infections using CD4-positive HeLa cells, the EnvY712A mutation impaired
50 munodeficiency virus (FIV) targets activated CD4-positive helper T cells preferentially, inducing an
51                                              CD4-positive human CEM-SS T-cell lines were generated wh
52  at IC(90)s, IC(99)s, or IC(> or = 99)s in a CD4-positive human lymphoblastoid cell line (H9 cells) a
53 locked cell fusion and infection with normal CD4-positive human target cells.
54 h leads to the expression of the CD4 gene in CD4-positive hybridoma cells and double-positive thymocy
55 rtantly, TIM-1 inhibits HIV-1 replication in CD4-positive Jurkat cells, despite its capability of up-
56 ion with intracellular localization in human CD4-positive Jurkat T cells.
57 s variants that grow to different extents in CD4-positive leukemic cell lines and that differ only at
58 creased IL-18BP production is a reduction in CD4-positive lymphocyte activation in response to IL-18
59 ral therapy was provided if participants had CD4-positive lymphocyte counts of fewer than 200 cells p
60 ty to cause syncytium formation or fusion in CD4-positive lymphocyte cultures.
61  contribution of these properties to in vivo CD4-positive lymphocyte depletion.
62 lly described between the T-cell receptor of CD4-positive lymphocytes and MHC II on antigen-presentin
63 deficiency virus type 1 (HIV-1) infection of CD4-positive lymphocytes is accompanied by acute cytopat
64 n lead to direct targeting of hepatocytes by CD4-positive lymphocytes, which form an immunologic syna
65 V-1 isolates resulted in the lysis of single CD4-positive lymphocytes.
66 lation and the enhancement of replication in CD4-positive lymphocytes.
67 mal ciliated respiratory epithelia and a CD8/CD4-positive lymphocytic infiltrate that peaked at 21 da
68  numbers of immune cells, including T cells (CD4-positive), macrophages, and mast cells, at all time
69                                              CD4-positive membrane vesicles (MV) were isolated under
70 s were developed and were shown to express a CD4 positive memory T cell phenotype.
71   These Dsg1-reactive FS T cells exhibited a CD4-positive memory T-cell phenotype and produced a T he
72 ence the development and selection of, e.g., CD4-positive, MHC class II-specific T cells.
73 th IL-15 for 1 week normalizes their hepatic CD4-positive natural killer cell content.
74  these Kupffer cell factors promotes hepatic CD4-positive natural killer cell depletion in ob/ob live
75 vers to lipopolysaccharide, why such hepatic CD4-positive natural killer cell depletion occurs is unc
76 in [IL]-12) or enhance (e.g., IL-15) hepatic CD4-positive natural killer cell viability.
77 tokine production and the hepatic content of CD4-positive natural killer cells were compared in ob/ob
78     The livers of ob/ob mice are depleted of CD4-positive natural killer cells, components of the inn
79 mice and partially replenishes their hepatic CD4-positive natural killer cells.
80                       Rather, infection of a CD4-positive precursor cell (CD4 positive/CD8 positive)
81 and replication in several cell lines and in CD4-positive primary lymphocytes.
82 ts of CD4 and replicate more aggressively in CD4-positive primary lymphocytes.
83 ased ratio of these cells to Foxp3-positive, CD4-positive regulatory T cells with sequential therapy.
84 uced tumoral infiltration of neutrophils and CD4 positive T cells, which can be explained by decrease
85                               Tumor-reactive CD4-positive T cell clones were isolated from TIL and te
86 s were highly specific and restricted to the CD4-positive T cell population.
87                      In the absence of GILT, CD4-positive T cell responses to Der p 1 are significant
88 ith a reduction in the number of circulating CD4-positive T cells (P=0.01), and reduced expression of
89                                    Activated CD4-positive T cells are essential in the early stages o
90                              Since activated CD4-positive T cells are involved in pathogenesis of var
91 l populations, as well as the percentages of CD4-positive T cells expressing IFN-gamma and of NKp46/C
92                           We also found that CD4-positive T cells in mice with preexisting immunity t
93 phoid organs, with preferential expansion of CD4-positive T cells in the recipient spleens.
94  and the cytopathicity of virus for infected CD4-positive T cells in this animal model of HIV-1 infec
95                                The number of CD4-positive T cells increased by 2.8-fold in MHC I-defi
96 s II and ICAM-1 (ProAd-ICAM) can drive naive CD4-positive T cells into cell cycle, but these T cells
97 to activate Ag-specific Th1 clones and naive CD4-positive T cells isolated from TCR transgenic mice.
98 t on the formation of either mature CD8- and CD4-positive T cells or granulocytes or macrophages, but
99 om patient 888 indicated that they contained CD4-positive T cells that recognized the autologous tumo
100       Dose-dependent inhibition of activated CD4-positive T cells to HIV-1 infection with both bindin
101 ntended to engage and render gluten-specific CD4-positive T cells unresponsive to further antigenic s
102             Previous studies have shown that CD4-positive T cells vary in a predictable manner over 2
103 ionships between cell types like B cells and CD4-positive T cells vary with tissue type.
104  to HIV-1 infection by challenging activated CD4-positive T cells with CCR5-binding and CXCR4-binding
105 rate that was primarily composed of CD3- and CD4-positive T cells, CD20-expressing B cells, macrophag
106  immunodominant epitopes for gluten-specific CD4-positive T cells.
107 s for antigen processing and presentation to CD4-positive T cells.
108 e 1 (HIV-1) infection is the gradual loss of CD4-positive T cells.
109 rment in the activation of these specialized CD4-positive T cells.
110 essed antigens to T cell receptors (TCRs) of CD4-positive T cells.
111  could not replicate in primary A. nancymaae CD4-positive T cells.
112 hey also had increased numbers of glomerular CD4-positive T cells.
113  as F4/80-positive macrophages/microglia and CD4-positive T cells.
114 ntigens from dying cells and present them to CD4-positive T cells.
115  marked decrease in the numbers of activated CD4-positive T cells.
116 C full-length cDNA are infectious in primary CD4-positive T cells.
117 quired for effective antigen presentation to CD4-positive T cells.
118 rogressive increase in their number of naive CD4-positive T cells.
119 issues are enriched in macrophages (MOs) and CD4-positive T cells; however, T helper-type cytokines s
120         Flow cytometric analysis showed that CD4-positive T lymphocyte division was specifically supp
121 lecule (VCAM-1), and MHC class II as well as CD4-positive T lymphocyte infiltration was detected by i
122                  The change in percentage of CD4-positive T lymphocytes (CD4%) was investigated in 10
123 essor or cytotoxic subset) predominated over CD4-positive T lymphocytes (helper cells) surrounding th
124                           Infection of human CD4-positive T lymphocytes by human immunodeficiency vir
125 creased on mononuclear leukocytes, including CD4-positive T lymphocytes from HIV-positive patients, c
126 ex (MHC) class II-restricted presentation to CD4-positive T lymphocytes occurs after they are interna
127 ion aged 5.7-12.0 weeks with a percentage of CD4-positive T lymphocytes of at least 25% were randomly
128 acterial lipopeptides that are recognized by CD4-positive T lymphocytes of Mycobacterium tuberculosis
129 les, as well as the subsequent activation of CD4-positive T lymphocytes.
130 ass II (MHC II) molecules for recognition by CD4-positive T lymphocytes.
131 ion of nef led to a substantial reduction in CD4-positive T-cell depletion and delayed kinetics of pl
132 lly, relevant doses of Ze-NO induce a dermal CD4-positive T-cell infiltrate and IFN-gamma secretion.
133 detected by reverse transcription-PCR in the CD4-positive T-cell line C8166, but not in peripheral bl
134 , characterised by a T-helper 1 (Th1) biased CD4-positive T-cell response and granuloma formation, fo
135 fection(1-3), but it remains unclear whether CD4-positive T-cell subsets with similar features exist
136  and early CD8-positive cytotoxic T-cell and CD4-positive T-helper cell responses directed toward HIV
137 troviral therapy (HAART) on the evolution of CD4-positive T-lymphocyte (CD4 cell) count among human i
138 s evaluated population- and individual-level CD4-positive T-lymphocyte (CD4 cell) count trajectories
139 with 77 nonusers on age, race, and pre-HAART CD4-positive T-lymphocyte (CD4+ cell) count and viral lo
140  tested semiannually to identify their first CD4-positive T-lymphocyte cell count below 200/microl; t
141 equency of measurement of HIV RNA levels and CD4-positive T-lymphocyte cell counts introduce a possib
142                                   The annual CD4-positive T-lymphocyte cell decline was less in untre
143 e (p = 0.10), low hemoglobin (p = 0.11), and CD4-positive T-lymphocyte count (p = 0.04).
144 men and how this effect differs depending on CD4-positive T-lymphocyte count.
145                                              CD4-positive, T-cell-enriched PECs contained only a very
146 to the inhibitory effects of the compound in CD4-positive target cells.
147  to protect against disorders with increased CD4-positive Th1 responses in animals.

 
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