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1.
Cell Biol Int ; 46(11): 1876-1885, 2022 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-35880847

RESUMO

Hematopoietic stem cells (HSCs) transplantation is considered a suitable treatment for malignant or nonmalignant hematological diseases. This study aims to investigate the HSCs homing factors in bone marrow (BM) donors of acute lymphoblastic leukemia (ALL) patients following granulocyte colony-stimulating factor (G-CSF) injection, as well as the G-CSF effects on BM transplantation quality in these patients. To mobilize HSCs into peripheral blood, G-CSF was used for ALL patient's BM donors. For HSCs counting, CD34+ cells were evaluated in analogous and autologous donors using flow cytometry. The expression of stem cell homing factors in CD34+ cells and peripheral blood mononuclear cells (PBMCs) were investigated using a real-time polymerase chain reaction. Finally, hematological factors after BM transplantation in ALL patients were assessed. According to our results, after G-CSF injection, the level of CD34+ HSCs was statistically increased. Besides, autologous donors showed a higher level of CD34+ cells compared to analogous donors before and after G-CSF injection. Additionally, a higher number of CD34+ HSCs was achieved in the autologous samples following G-CSF injection. Furthermore, after G-CSF injection, the expression of matrix metalloproteinase (MMP)-2, MMP-9 was increased; while, stromal cell-derived factor 1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 expression were decreased. Moreover, the expression of C-X-C chemokine receptor type 4, lymphocyte function-associated antigen 1, and very late antigen-4 in CD34+ cells and PBMCs were decreased. BM transplantation on Day 90 also caused an increased level of white blood cells, red blood cells, and platelets as compared to the first day; however, no statistical differences were observed in hemoglobin level. In conclusion, G-CSF by altering the expression of HSCs homing factors in ALL donors improves BM transplantation quality in ALL patients.


Assuntos
Molécula 1 de Adesão Intercelular , Leucemia-Linfoma Linfoblástico de Células Precursoras , Antígenos CD34 , Moléculas de Adesão Celular , Quimiocina CXCL12 , Fator Estimulador de Colônias de Granulócitos/farmacologia , Células-Tronco Hematopoéticas , Hemoglobinas , Humanos , Integrina alfa4beta1 , Leucócitos Mononucleares , Metaloproteinase 9 da Matriz , Leucemia-Linfoma Linfoblástico de Células Precursoras/terapia , Receptores de Quimiocinas , Molécula 1 de Adesão de Célula Vascular
2.
Iran J Allergy Asthma Immunol ; 14(5): 519-25, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26742441

RESUMO

Tetanus is caused by the tetanus neurotoxin (TeNT), a 150 kDa single polypeptide molecule which is cleaved into active two-chain molecules composed of a 50 kDa N-terminal light (L) and a 100 kDa C-terminal heavy (H) chains. Fragment C is further subdivided into two subdomains: the proximal HCN  subdomain and the extreme carboxy subdomain, HCC. HCC is considered as an immunodominant part of TeNT and is responsible for TeNT binding activity to neurons.In the present study, we investigated the ability of recombinant HCC(r HCC) to induce T cell activation. Our results showed that recombinant HCC has a stimulatory effect on IFN-γ secretion by T cells after 48h co-incubation in the presence of anti-TLR-2 Ab. Also, Hcc can induce the expression of CD69 on T cells.Our finding indicated that stimulatory effects of HCC on T cells are TLR-2 independent and anti-TLR-2 inhibitory antibody fails to neutralize HCC stimulatory effects on T cells.Furthermore, HCC  is critical for immunogenic activity of TeNT and is able to induce T cells through TLR-2 independent pathway.


Assuntos
Interferon gama/efeitos dos fármacos , Ativação Linfocitária/efeitos dos fármacos , Bloqueadores Neuromusculares/farmacologia , Fragmentos de Peptídeos/farmacologia , Linfócitos T/efeitos dos fármacos , Toxina Tetânica/farmacologia , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Anticorpos/imunologia , Anticorpos/farmacologia , Antígenos CD/efeitos dos fármacos , Antígenos CD/imunologia , Antígenos de Diferenciação de Linfócitos T/efeitos dos fármacos , Antígenos de Diferenciação de Linfócitos T/imunologia , Humanos , Interferon gama/metabolismo , Interleucina-4/metabolismo , Lectinas Tipo C/efeitos dos fármacos , Lectinas Tipo C/imunologia , Linfócitos T/imunologia , Linfócitos T/metabolismo , Receptor 2 Toll-Like/imunologia , Fator de Necrose Tumoral alfa/metabolismo
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