Increased CD4+ and CD8+ effector memory T cells in patients with aplastic anemia

Hu, Xiaojing; Gu, Yan; Wang, Yingxue; Cong, Yaqin; Qu, Xun; Xu, Cheng-Hui

doi:10.3324/haematol.13412

Cited by 22 publications

(16 citation statements)

References 11 publications

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“…Within the CD4 + or CD8 + T cell compartments, AA patients showed decreased CD4 + or CD8 + TN frequency ( p < 0.05, Fig. 1B), compared to controls, consistent with previous reports (11). CD4 + TE frequency was very low in the CD4 + T cell compartment in both AA and controls, but CD8 + TE frequency was higher among CD8 + T cells in both.…”

Section: Resultssupporting

confidence: 92%

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Memory Stem T Cells in Autoimmune Disease: High Frequency of Circulating CD8+ Memory Stem Cells in Acquired Aplastic Anemia

Hosokawa

Muranski

Feng

et al. 2016

The Journal of Immunology

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Memory stem T cells (TSCMs) constitute a long-lived, self-renewing lymphocyte population essential for the maintenance of functional immunity. Hallmarks of autoimmune disease pathogenesis are abnormal CD4+ and CD8+ T cell activation. We investigated the TSCM subset in 55, 34, 43, and 5 patients with acquired aplastic anemia (AA), autoimmune uveitis, systemic lupus erythematosus, and sickle cell disease, respectively, as well as in 41 age-matched healthy controls. CD8+ TSCM frequency was significantly increased in AA compared with healthy controls. An increased CD8+ TSCM frequency at diagnosis was associated with responsiveness to immunosuppressive therapy, and an elevated CD8+ TSCM population after immunosuppressive therapy correlated with treatment failure or relapse in AA patients. IFN-γ and IL-2 production was significantly increased in various CD8+ and CD4+ T cell subsets in AA patients, including CD8+ and CD4+ TSCMs. CD8+ TSCM frequency was also increased in patients with autoimmune uveitis or sickle cell disease. A positive correlation between CD4+ and CD8+ TSCM frequencies was found in AA, autoimmune uveitis, and systemic lupus erythematosus. Evaluation of PD-1, CD160, and CD244 expression revealed that TSCMs were less exhausted compared with other types of memory T cells. Our results suggest that the CD8+ TSCM subset is a novel biomarker and a potential therapeutic target for AA.

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Section: Resultssupporting

confidence: 92%

“…The percentages of CD4 + and CD8 + TEM subsets are increased in peripheral blood (PB) and BM of AA patients (11). Elevated TEM cells with potent effector capacity may relate to abnormal immunity in AA.…”

Section: Introductionmentioning

confidence: 99%

Memory Stem T Cells in Autoimmune Disease: High Frequency of Circulating CD8+ Memory Stem Cells in Acquired Aplastic Anemia

Hosokawa

Muranski

Feng

et al. 2016

The Journal of Immunology

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“…Hence, an increase of dual expressing (CD45RO/CD45RA) in the pool of circulating CD8 cells might explain the simultaneous increases observed in both CD8 + CD45RO and CD8 + CD45RA subpopulations in our patients. On the other hand, the greater frequency of circulating CD8 + CD45RA cells in patients with NASH might correspond to CD8 T memory cells CD45RA-positive denominated "effector memory RA" [36]. Each one of both circumstances refers to a greater pool of CD8 T cells undergoing activation in patients than controls.…”

Section: Discussionmentioning

confidence: 98%

The Role of Innate Cells Is Coupled to a Th1-Polarized Immune Response in Pediatric Nonalcoholic Steatohepatitis

et al. 2012

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“…This indicates T cells in AA patients can suppress hemopoiesis. Further studies demonstrated AA patients not only had abnormal T cell population, the subgroup distribution, function, phenotype, and activated state also changed significantly [18][19][20][21] .…”

Section: Discussionmentioning

confidence: 99%

Proliferation and apoptosis of bone marrow CD4+ T cells in patients with aplastic anemia and impacts of the secreted cytokines on hematopoietic stem cells from umbilical cord blood

Zheng

Sun

Zhou

et al. 2010

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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Recent studies indicate that immune-associated aplastic anemia (AA) resembles such autoimmune diseases as insulin-dependent diabetes and chronic autoimmune thyroiditis that belong to organ-specific autoimmune diseases. Many independent investigation groups have successfully isolated the pathopoiesis-associated T cell clone causing hematopoiesis failure with a CD4 phenotype from peripheral blood and bone marrow (BM) in AA patients. In the current study, BM CD4(+) T cells were isolated from AA patients and healthy controls with immunomagnetic beads sorting, and proliferation capability, apoptosis features and the impacts of their secreted cytokines on hematopoiesis stem/progenitor cells were compared between them. By (3)H-TdR method, CD4(+) T cells in AA group presented more enhanced proliferative activity. The stimulation index in control group and AA group was 1.47+/-0.24, and 2.51+/-0.34 respectively (P<0.01). After BM CD4(+) T cells were induced by high concentration of CD3 monoclonal antibody for 18 h, evident apoptosis cells could be seen under the electron microscope in both control group and AA group. Flow cytometry revealed that apoptosis rates in the early and late stages of AA group were significantly higher than in control group (P<0.01). Early-stage apoptosis rate in control and AA groups was (6.85+/-1.48)% and (16.98+/-4.40)%, and late-stage apoptosis rate in control group and AA group was (2.65+/-1.57)% and (7.74+/-0.83)%, respectively (P<0.01). The CFU-GM count in AA group and control group was (74.50+/-9.50)/10(4) cells and (124.25+/-19.80)/10(4) cells respectively under an inverted microscope (P<0.01), and the expression levels of CyclinD3 mRNA and protein in cord blood CD34(+) cells were both down-regulated induced by BM CD4(+) T cell culture supernatant in AA patients. These results indicate that BM CD4(+) T cells of AA patients are likely in an abnormally proliferative, and activated state which can correlate intimately with AA hematopoiesis damage. BM CD4(+) T cells in AA patients can secret some soluble cytokines that can inhibit proliferation of hematopoietic stem cells by suppressing the expression of Cyclin D3, resulting in hematopoiesis failure.

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Increased CD4+ and CD8+ effector memory T cells in patients with aplastic anemia

Cited by 22 publications

References 11 publications

Memory Stem T Cells in Autoimmune Disease: High Frequency of Circulating CD8+ Memory Stem Cells in Acquired Aplastic Anemia

Memory Stem T Cells in Autoimmune Disease: High Frequency of Circulating CD8+ Memory Stem Cells in Acquired Aplastic Anemia

The Role of Innate Cells Is Coupled to a Th1-Polarized Immune Response in Pediatric Nonalcoholic Steatohepatitis

Proliferation and apoptosis of bone marrow CD4+ T cells in patients with aplastic anemia and impacts of the secreted cytokines on hematopoietic stem cells from umbilical cord blood

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