Soluble HLA‐G Molecules Induce Apoptosis in Natural Killer Cells

Lindaman, Amy; Dowden, Amy; Zavazava, Nicholas

doi:10.1111/j.1600-0897.2006.00395.x

Cited by 31 publications

(24 citation statements)

References 41 publications

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“…CD34 ϩ -derived hematopoietic progeny (CFU-GEMM) culture supernatants were purified by affinity chromatography (HiTrap Streptavidin HP Column; Amersham-Pharmacia-GE Healthcare, Uppsala, Sweden) with a biotinylated anti-HLA-G moAb (MEM-G9; Exbio, Praha, Czech Republic) [24], that is specific for both HLA-G1 and -G5 isoforms. Elution was performed with 50 mmol/l ammonium acetate, 0.5 mol/l NaCl, pH 4.0 accordingly with the producer.…”

Section: Shla-g Purificationmentioning

confidence: 99%

Umbilical cord blood CD34+cell–derived progeny produces human leukocyte antigen–G molecules with immuno-modulatory functions

et al. 2012

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Section: Shla-g Purificationmentioning

confidence: 99%

Umbilical cord blood CD34+cell–derived progeny produces human leukocyte antigen–G molecules with immuno-modulatory functions

et al. 2012

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“…These soluble HLA class-I (sHLA-I) and class-II (sHLA-II) molecules may have immunomodulatory function [2-4]. Normal individuals have stable concentrations of sHLA-I and sHLA-II in their serum [1].…”

Section: Introductionmentioning

confidence: 99%

Saliva soluble HLA as a potential marker of response to interferon-β1a in multiple sclerosis: A preliminary study

Minagar

Adamashvili

Kelley

et al. 2007

J Neuroinflammation

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Objective: Potential surrogate markers of disease activity, including response to therapy, are particularly important in a neurological disorder such as multiple sclerosis (MS) which often has a fluctuating course. Based upon previous studies in our laboratory, we hypothesized that measurement of soluble HLA (sHLA) molecules class II in saliva of MS patients can serve as marker of therapeutic response to high dose interferon beta-1a. Methods:We measured the expression patterns of sHLA-II in saliva in 17 patients with relapsing/ remitting MS and compared the results to clinical course and brain MRI. For comparison purposes we also assayed the saliva sHLA-II levels in 53 normal control subjects. Solid phase ELISA was used for measurement of sHLA-I and sHLA-II concentrations at baseline and after three and six months of treatment with high dose interferon beta-1a (IFN β-1a). Results:The mean saliva sHLA-ll levels in MS patients was significantly higher than normal controls (354 ± 42 unit/mL vs. 222 ± 18 unit/mL, t= 8.16, p < 0.003). Comparison of saliva sHLA-II values before and after treatment with IFN β-1a revealed a consistent increase in mean concentration. The increase in saliva sHLA-II values (354 ± 42 unit/mL at baseline versus 821 ± 86 unit/mL at 3 months and 776 ± 63 unit/mL at 6 months, in unit/mL, p < 0.001 for both comparisons) was associated with a stable clinical course and a decline of the number of contrast-enhancing lesions on brain MRI. Comparison of the volume of T2-weighted lesions and the number of black holes on T1-weighted images did not reveal any significant changes (during pre-treatment versus posttreatment month 6) or any correlations with saliva sHLA-II levels. Saliva sHLA-I levels were not detectable. Conclusion:Serial measurement of saliva sHLA-II may serve as a potential marker of therapeutic response to IFN β-1a. Larger clinical studies involving more RRMS patients over longer periods of time are needed to further test the significance and value of saliva sHLA-II as an accurate marker of therapeutic response to beta-interferons.

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“…16,17 HLA-G molecules inhibit NK cell-mediated cytotoxicity through down-regulation of perforin and Stat3, 18 and they also may induce fratricide killing of NK cells. 19 More recently, it has been demonstrated that sHLA-G inhibits NK-cell-mediated lysis, impairing actin reorganization and perforin granule polarization toward target cells. 20 Moreover, the impaired cytoskeletal reorganization affects CD2 localization in late NK-to-target cell immune synapse.…”

Section: Introductionmentioning

confidence: 99%

Soluble HLA-G dampens CD94/NKG2A expression and function and differentially modulates chemotaxis and cytokine and chemokine secretion in CD56bright and CD56dim NK cells

Morandi

Ferretti

Castriconi

et al. 2011

Blood

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Soluble HLA-G (sHLA-G) inhibits natural killer (NK) cell functions. Here, we investigated sHLA-G–mediated modulation of (1) chemokine receptor and NK receptor expression and function and (2) cytokine and chemokine secretion in CD56bright and CD56dim NK cells. sHLA-G-treated or untreated peripheral blood (PB) and tonsil NK cells were analyzed for chemokine receptor and NK receptor expression by flow cytometry. sHLA-G down-modulated (1) CXCR3 on PB and tonsil CD56bright and CD56dim, (2) CCR2 on PB and tonsil CD56bright, (3) CX3CR1 on PB CD56dim, (4) CXCR5 on tonsil CD56dim, and (5) CD94/NKG2A on PB and tonsil CD56bright and CD56dim NK cells. Such sHLA-G–mediated down-modulations were reverted by adding anti–HLA-G or anti–ILT2 mAbs. sHLA-G inhibited chemotaxis of (1) PB NK cells toward CXCL10, CXCL11, and CX3CL1 and (2) PB CD56bright NK cells toward CCL2 and CXCL10. IFN-γ secretion induced by NKp46 engagement was inhibited by NKG2A engagement in untreated but not in sHLA-G–treated NK cells. sHLA-G up-regulated secretion of (1) CCL22 in CD56bright and CD56dim and (2) CCL2, CCL8, and CXCL2-CXCL3 in CD56dim PB NK cells. Signal transduction experiments showed sHLA-G–mediated down-modulation of Stat5 phosphorylation in PB NK cells. In conclusion, our data delineated novel mechanisms of sHLA-G–mediated inhibition of NK-cell functions.

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Soluble HLA‐G Molecules Induce Apoptosis in Natural Killer Cells

Cited by 31 publications

References 41 publications

Umbilical cord blood CD34+cell–derived progeny produces human leukocyte antigen–G molecules with immuno-modulatory functions

Umbilical cord blood CD34+cell–derived progeny produces human leukocyte antigen–G molecules with immuno-modulatory functions

Saliva soluble HLA as a potential marker of response to interferon-β1a in multiple sclerosis: A preliminary study

Soluble HLA-G dampens CD94/NKG2A expression and function and differentially modulates chemotaxis and cytokine and chemokine secretion in CD56bright and CD56dim NK cells

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