CD11bGr-1 cells that are increased in the lungs of a Mycobacterium (M) tuberculosis-infection mouse model have the characteristics of monocytic (M)-myeloid-derived suppressor cells (MDSCs) and harbor M.tuberculosis. Interestingly, a high number of M-MDSCs have also been observed in skin lesions of patients with lepromatous leprosy. We hypothesized that CD11bGr-1 cells might be involved in the pathogenesis of leprosy, as they are in tuberculosis. In the current study, we investigated the issue of whether CD11bGr-1 cells accumulate in Mycobacterium (M) leprae-induced granulomas of the footpad skin of nude mice. Our results show that CD11bGr-1 cells began to accumulate in the 7-month-old M.leprae-induced granulomas and were replaced by other leukocytes, including CD11bGr-1 over time during M.leprae infections. CD11b Gr-1 cells expressed the surface markers of M-MDSC, Ly6C and Ly6G. In addition, CD11bGr-1 cells have the nuclei of a mononuclear cell type and expressed higher levels of arginase 1 (Arg1) and inducible NO synthetase (iNOS). Furthermore, they showed a higher infection rate by M.leprae. Taken together, our results indicate that the inoculation with M.leprae induced an accumulation of CD11b Gr-1 at a relatively early stage, 7-month-old M.leprae-induced granulomas, and that CD11bGr-1 have the characteristics of M-MDSC and may act as a reservoir for M.leprae.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.tube.2023.102345 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
IL-20 contributes to low grade inflammation and weight gain in the Psammomys obesus.
Int Immunopharmacol
April 2017
Hagedorn Research Institute, DK-2820 Gentofte, Denmark. Electronic address:
The metabolic syndrome has been demonstrated in gene deficient animals, e.g. db/db mice, to include a systemic inflammation leading to insulin resistance, obesity and type 2 diabetes (T2D).
View Article and Find Full Text PDFInhibition of histone deacetylase 6 restores innate immune cells in the bone marrow in a lethal septic model.
J Trauma Acute Care Surg
January 2016
From the Department of Surgery, University of Michigan Hospital, Ann Arbor, Michigan.
Background: We have previously demonstrated that Tubastatin A, a selective inhibitor of histone deacetylase 6 (HDAC6), improves survival and increases circulating monocyte count and bacterial clearance in a lethal model of cecal ligation and puncture (CLP) in mice. The aim of the present study was to characterize the effects of inhibition of HDAC6 on the bone marrow cell population.
Methods: C57BL/6J mice were subjected to CLP and, 1 hour later, given an intraperitoneal injection of either Tubastatin A (70 mg/kg) dissolved in DMSO or DMSO alone (n = 9 per group).
Long-lasting complete regression of established mouse tumors by counteracting Th2 inflammation.
J Immunother
May 2013
Department of Pathology, Harborview Medical Center, University of Washington, Seattle, WA 98104-2499, USA.
Mice with intraperitoneal ID8 ovarian carcinoma or subcutaneous SW1 melanoma were injected with monoclonal antibodies (mAbs) to CD137PD-1CTLA4 7-15 days after tumor initiation. Survival of mice with ID8 tumors tripled and >40% of mice with SW1 tumors remained healthy >150 days after last treatment and are probably cured. Therapeutic efficacy was associated with a systemic immune response with memory and antigen specificity, required CD4 cells and involved CD8 cells and NK cells to a less extent.
View Article and Find Full Text PDFAgonistic Anti-CD137 Monoclonal Antibody Treatment Induces CD11bGr-1 Myeloid-derived Suppressor Cells.
Immune Netw
June 2010
Laboratory of Immunology, Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea.
CD137 (4-1BB/tnfrsf9) has been shown to co-stimulate T cells. However, agonistic anti-CD137 monoclonal antibody (mAb) treatment can suppress CD4(+) T cells, ameliorating autoimmune diseases, whereas it induces activation of CD8(+) T cells, resulting in diverse therapeutic activity in cancer, viral infection. To investigate the CD137-mediated T cell suppression mechanism, we examined whether anti-CD137 mAb treatment could affect CD11b(+)Gr-1(+) myeloid-derived suppressor cells (MDSCs).
View Article and Find Full Text PDFCpG-induced myeloid CD11b+Gr-1+ cells efficiently suppress T cell-mediated immunoreactivity and graft-versus-host disease in a murine model of allogeneic cell therapy.
Biol Blood Marrow Transplant
September 2008
The International Centre for Cell Therapy and Cancer, Tel Aviv (Souraski) Medical Center, Tel Aviv 64239, Israel.
Transplantation of mismatched allografts in irradiated recipients results in lethal graft- versus-host disease (GVHD). In our study, pretransplantation donor treatment with CpG, administered either alone or emulsified in incomplete Freund's adjuvant, efficiently prevented GVHD in sublethally irradiated recipients of haploidentical (H-2(b) into H-2(b/d)) and fully mismatched (H-2(b) into H-2(d)) allografts. CpG treatment of donor mice caused an accumulation of double-positive CD11bGr-1 cells in their blood and spleens, whereas treatment with CpG+IFA resulted in an even greater accumulation of these cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!