Increased frequency of CD56Bright NK‐cells, CD3−CD16+CD56− NK‐cells and activated CD4+T‐cells or B‐cells in parallel with CD4+CDC25High T‐cells control potentially viremia in blood donors with HCV

Zarife, Maria Alice Sant'Anna; Reis, Eliana A. G.; Carmo, Theomira Mauadie Azevedo; Lopes, Gisele Barreto; Brandão, Emilia Carolina Malafaia; Silva, Helder Reis; Santana, Nelma; Martins‐Filho, Olindo Assis; Reis, Mitermayer Galvão dos

doi:10.1002/jmv.21340

Cited by 27 publications

(21 citation statements)

References 53 publications

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“…The current study found a reduced frequency of NK cells in post-hepatitis cirrhosis which is in agreement with previous research indicating an inadequacy of innate host response and inefficient initiation of adaptive immune response [9, 10]. We also showed that no difference was found between the nonviremic and viremic groups, which is inconsistent with the results of Zarife et al [7]. Different methodologies, including the CD45 labeling, smaller sample sizes, and differences in severity of disease, might explain why some of the findings in these studies differed from ours.…”

Section: Discussionsupporting

confidence: 78%

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Immunologic Characterization of Posthepatitis Cirrhosis Caused by HBV and HCV Infection

Jiang

Jin

et al. 2010

Journal of Biomedicine and Biotechnology

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No specific treatment can reverse the liver injury in cirrhosis. This study aims to characterize immune status and correlations between cirrhosis induced by HBV and HCV. Phenotypes of peripheral blood lymphocyte subsets (T, NK, regulatory T cells) and Th cytokine secretion were analyzed using flow cytometry in 42 HBV-cirrhotic and 40 HCV-cirrhotic patients. Cirrhotic patients had a lower proportion of CD3+CD8+T cells and NK cells, while the proportion of CD3+CD4+T cells and Treg cells were higher than those of healthy controls. The levels of Th2 cytokine (IL-6) in cirrhotic patients were increased, while only the Th1 cytokine (IFN-γ) increased in HBV-cirrhotic patients. These findings show that there is no difference between the cirrhotic groups except in the IFN-γ level. In cirrhosis, defects in innate, adaptive immune cells are likely regardless of which virus is involved. A cytokine imbalance may play a role in the development of posthepatitic cirrhosis.

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Section: Discussionsupporting

confidence: 78%

“…Following incubation, erythrocytes were lysed using 1 ml FACS lysing solution (eBioscience Inc., USA). The cells were washed twice with 2 ml PBS buffer [7]. …”

Section: Methodsmentioning

confidence: 99%

Immunologic Characterization of Posthepatitis Cirrhosis Caused by HBV and HCV Infection

Jiang

Jin

et al. 2010

Journal of Biomedicine and Biotechnology

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“…Significant alterations in NK subsets in patients with chronic HCV infection compared with individuals who resolved the infection and healthy controls have been described (Golden-Mason et al, 2006). Phenotypic analysis of NK cells in HCV non-viremic and viremic groups suggests that elevated levels of CD56 Bright NK cells, together with pre-NK cells and activated CD4 + T-cells in combination with CD4 + CD25 High T-cells, is associated with viremia control (Zarife et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Protective KIR–HLA interactions for HCV infection in intravenous drug users

Zúñiga

Romero

Azócar³

et al. 2009

Molecular Immunology

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Intravenous drug use has become the principal route of hepatitis C virus (HCV) transmission due to the sharing of infected needles. In this study, we analyzed the distribution of HLA-KIR genotypes among 160 Puerto Rican intravenous drug users (IDUs) with HCV infection and 92 HCV-negative Puerto Rican IDUs. We found a significant association between the presence of different combinations of KIR inhibitory receptor genes (KIR2DL2 and/or KIR2DL3, pC = 0.01, OR = 0.07; KIR2DL2 and/or KIR2DL3+KIR2DS4, pC = 0.01, OR = 0.39) and HLA-C1 homozygous genotypes (HLA-C1+KIR2DS4, pC = 0.02, OR = 0.43; HLA-C1+KIR2DL2+KIR2DS4, pC = 0.02, OR = 0.40) together with the activating receptor KIR2DS4 (HLA-C1+KIR2DS4+KIR2DL3 and/or KIR2DL2, pC = 0.004, OR = 0.38) with protection from HCV infection. Our findings in HCV-infected and noninfected IDUs suggest an important role for KIRs (KIR2DL2 and KIR2DL3) with group HLA-C1 molecules, in the presence of activating KIR2DS4, in protection from HCV infection. These results

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“…90%) of NK cells are CD56 dim , whereas approximately 10% of NK cells are CD56 bright [1]. NK cells lacking CD56 expression are rare in healthy donors, were originally described in HIV-infected individuals [21,22] and have more recently been found at elevated levels in other chronic infectious diseases, such as hepatitis C [23,24] and Chagas disease [25]. However, in these settings, NK cells lacking CD56 expression are functionally defective as they display decreased levels of activating receptors and fail to kill target cells.…”

Section: Discussionmentioning

confidence: 99%

Expansion of CD56-Negative, CD16-Positive, KIR-Expressing Natural Killer Cells after T Cell-Depleted Haploidentical Hematopoietic Stem Cell Transplantation

et al. 2011

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The main functions of natural killer (NK) cells are early protection against viruses or tumor cells and production of cytokines that regulate immune functions. The present study assessed the role of different NK subsets in exerting graft-versus-leukemia effects in recipients of human leukocyte antigen (HLA) haploidentical hematopoietic transplants and monitored for the first time CD3–/CD56– lymphocyte expansion. CD3–/CD56– cells expressed NK cell-associated molecules, such as CD16, NKp46, NKp30, CD244 (2B4), CD161, and killer cell immunoglobulin-like receptors. CD3–/CD56– cells further exhibited the classical functional characteristics of NK cells: cytolysis of target cells lacking HLA class I, antibody-dependent cellular cytotoxicity and cytokine production. These results demonstrate that CD56– NK cells are functional, recognize missing self and, like their CD56+ counterparts, may contribute to graft-versus-leukemia reactions.

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Increased frequency of CD56^Bright NK‐cells, CD3⁻CD16⁺CD56⁻ NK‐cells and activated CD4⁺T‐cells or B‐cells in parallel with CD4⁺CDC25^High T‐cells control potentially viremia in blood donors with HCV

Cited by 27 publications

References 53 publications

Immunologic Characterization of Posthepatitis Cirrhosis Caused by HBV and HCV Infection

Immunologic Characterization of Posthepatitis Cirrhosis Caused by HBV and HCV Infection

Protective KIR–HLA interactions for HCV infection in intravenous drug users

Expansion of CD56-Negative, CD16-Positive, KIR-Expressing Natural Killer Cells after T Cell-Depleted Haploidentical Hematopoietic Stem Cell Transplantation

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