Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0393754 (
HSA
)
2,996
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Infection of T cells with HIV-1 induces loss of CD4 and HLA class I from the cell surface. In the present article we have investigated whether changes in expression of other cell surface molecules could be related to HIV infection. To detect HIV-infected cells at the single-cell level, peripheral blood lymphocytes were infected in vitro with HIV-
HSA
, a reporter virus encoding the murine heat-stable antigen. Expression of
HSA
on activated primary lymphocytes was an efficient indicator of productive infection. Expression of the majority of the cell surface proteins studied was unaffected by HIV infection (HLA class I, II, CD11a, CD18, CD25, CD27, CD28, CD29, CD30, CD31, CD38, CD44, CD45R0, CD49d, CD57, CD94, CD95, and CXCR4). However, phenotypic changes specific to the productively infected cells were detected. Expression of the CD4 molecule was progressively lost and this was closely associated with loss of
CD62L
expression, a molecule involved in T cell homing into the lymph nodes. By contrast, T cells productively infected with this T-tropic reporter virus were enriched for CD54, and for CCR5, the main coreceptor for M-tropic viruses. Given the roles of
CD62L
, CD54, and CCR5 in lymphocyte trafficking, these results suggest that cells productively infected with HIV might have altered homing patterns in vivo.
...
PMID:Altered expression of CD4, CD54, CD62L, and CCR5 in primary lymphocytes productively infected with the human immunodeficiency virus. 1002 48
T cell emigration from the thymus is essential for immunological homeostasis. While stromal cell-produced sphingosine-1-phosphate (S1P) has been shown to promote thymocyte egress
via
the S1P receptor, S1PR1, the significance of S1P/S1PR1 signaling in the thymic stromal cells that surround T cells remains unclear. To address this issue, we developed conditional knockout mice (
Lyve1-CRE/S1pr1
f/f
mice) in which
S1pr1
was selectively targeted in cells expressing the lymphatic endothelial cell marker, Lyve1. In these mice, T cells were significantly reduced in secondary lymphoid tissues, and
CD62L
+
mature CD4 and CD8 single-positive (SP) T cells accumulated in the medulla failed to undergo thymus egress. Using a
Lyve1
reporter strain in which Lyve1 lineage cells expressed tdTomato fluorescent protein, we unexpectedly found that a considerable proportion of the thymocytes were fluorescently labeled, indicating that they belonged to the Lyve1 lineage. The CD4 and CD8 SP thymocytes in
Lyve1-CRE/S1pr1
f/f
mice exhibited an egress-competent phenotype (
HSA
low
,
CD62L
high
, and Qa-2
high
), but were CD69
high
and lacked S1PR1 expression. In addition, CD4 SP thymocytes from these mice were unable to migrate to the periphery after their intrathymic injection into wild-type (WT) mice. In contrast, WT T cells could migrate to the periphery in both WT and
Lyve1-CRE/S1pr1
f/f
thymuses. These results demonstrated that thymocyte egress is mediated by T cell-expressed, but not stromal cell-expressed, S1PR1 and caution against using the
Lyve1-CRE
system for selectively gene deletion in lymphatic endothelial cells.
...
PMID:Thymocytes in
Lyve1-CRE/S1pr1
f/f
Mice Accumulate in the Thymus due to Cell-Intrinsic Loss of Sphingosine-1-Phosphate Receptor Expression. 2787 75
