Impaired T cell capping and receptor regeneration in active systemic lupus erythematosus. Evidence for a disorder intrinsic to the T lymphocyte.

Kammer, Gary M.

doi:10.1172/jci111128

Cited by 45 publications

(27 citation statements)

References 33 publications

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“…What exactly causes the pooling of the low levels of the chain to membrane lipid rafts in SLE T cells and the functional role of this phenomenon remain enigmatic. It has been previously reported that SLE T cells have impaired capping and lateral mobility of receptors (65). Therefore, it is tempting to speculate that intrinsic abnormalities in the membrane could be responsible for the differential distribution of the decreased chain in SLE T cells.…”

Section: Discussionmentioning

confidence: 96%

Abnormal expression of various molecular forms and distribution of T cell receptor ? chain in patients with systemic lupus erythematosus

Nambiar

Enyedy

Fisher

et al. 2002

Arthritis & Rheumatism

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Section: Discussionmentioning

confidence: 96%

Abnormal expression of various molecular forms and distribution of T cell receptor ? chain in patients with systemic lupus erythematosus

Nambiar

Enyedy

Fisher

et al. 2002

Arthritis & Rheumatism

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“…At 30 minutes, only 60% of T cells were able to cap CD3, CD4, and CD8 molecules; 40% of T cells did not cap ( Figure ID; CD4 and CD8 not shown). This result is in contrast to our initial findings that 75-90% of T cells capped during inactive disease (23). In that study, we evaluated 6 patients during a period of active SLE and during a period of inactive SLE; those 6 patients were included in the present study of inactive disease.…”

Section: Impaired Capping Of T Cells From Patients With Inactive Slementioning

confidence: 67%

“…Although subjects who participated in this study had clinically inactive SLE, all patients had previously had active disease. Six of the patients had been studied previously, during episodes of active SLE (23). Of the remaining 8 patients, 6 had also been studied previously, during periods of inactive disease (24).…”

Section: Methodsmentioning

confidence: 99%

“…The criteria used to determine the activity of SLE have been described elsewhere (23). All patients were in clinical remission, as judged by the absence of clinical symptoms and signs, for an interval of at least 3 months.…”

Section: Methodsmentioning

confidence: 99%

“…The mean duration of clinical remission was 12 months (range 4-32 months). For the purposes of this study, patients with inactive disease could have an antinuclear antibody titer 2 1:40, normocomplementemia, or hypocomplementemia (as judged by reduced levels of C4), but did not have anti-double-stranded DNA antibody (23).…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Impaired mobility of human t lymphocyte surface molecules during inactive systemic lupus erythematosus. relationship to a defective camp pathway

Mitchell

1988

Arthritis & Rheumatism

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The T lymphocytes of patients with active systemic lupus erythematosus (SLE) exhibit impaired capping of the surface molecules CD3, CD4, and CDS and a defective CAMP-dependent pathway. Since the mobility of these molecules is regulated in part by CAMP, we sought to determine whether there is a specific defect(s) along the T cell cAMP pathway that contributes to the persistent capping disorder observed during inactive SLE. The data suggest that a defect may exist at the level of CAMP-dependent protein kinase activation or at a point distally. We propose that a disorder of CAMPdependent protein kinase activity might account for the defect of capping observed in both the CD3,CD4 (helperlinducer) and CD3,CDS (suppressor) subsets observed in SLE. (2-14), the genesis of the aberrant immune response remains uncertain. It has been demonstrated that autoantibodies directed against cell surface molecules of mononuclear cells can modify the immune response in SLE by interfering with interactions between cells (15). Systemic lupus erythematosus (SLE) is characterized by disordered humoral and cellular immunity ( I ) . Although several functional immune defects of mononuclear cells have been identified

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High prevalence of T cell type I protein kinase a deficiency in systemic lupus erythematosus

Kammer

1999

Arthritis & Rheumatism

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Impaired T cell capping and receptor regeneration in active systemic lupus erythematosus. Evidence for a disorder intrinsic to the T lymphocyte.

Cited by 45 publications

References 33 publications

Abnormal expression of various molecular forms and distribution of T cell receptor ? chain in patients with systemic lupus erythematosus

Abnormal expression of various molecular forms and distribution of T cell receptor ? chain in patients with systemic lupus erythematosus

Impaired mobility of human t lymphocyte surface molecules during inactive systemic lupus erythematosus. relationship to a defective camp pathway

High prevalence of T cell type I protein kinase a deficiency in systemic lupus erythematosus

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