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Signal-Transducing Adaptor Protein-2 Governs Recovery of B Lineage Lymphocytes during hematopoietic stress.

ABSTRACT: Signal-Transducing Adaptor Protein-2 Governs Recovery of B Lineage Lymphocytes during hematopoietic stress.

PROVIDER: PRJNA525841 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8690200.fastq.gz	Fastqsanger.gz
	SRR8690201.fastq.gz	Fastqsanger.gz
	SRR8690202.fastq.gz	Fastqsanger.gz
	SRR8690203.fastq.gz	Fastqsanger.gz
	SRR8690204.fastq.gz	Fastqsanger.gz

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Signal-Transducing Adaptor Protein-2 Governs Recovery of B Lineage Lymphocytes during hematopoietic stress.

Project description:Signal-transducing adaptor protein-2 (STAP-2) was discovered as a c-fms/M-CSFR interacting protein and subsequently found to function as an adaptor of signaling or transcription factors. These include STAT5, MyD88 and IB kinase (IKK) in macrophages, mast cells and T cells. There is additional information about roles in several types of malignant diseases including chronic myeloid leukemia, but none concerning B lineage lymphocytes. We have now exploited gene targeted and transgenic mice to address this issue and learned that it is not required under normal, steady-state conditions. However, recovery of B cells following transplantation was augmented in the absence of STAP-2. This appeared to be restricted to cells of this lineage and myeloid rebound was unremarkable. Furthermore, all hematological parameters were normal once recovery from transplantation was complete. Overexpression of STAP-2 specifically in lymphoid cells resulted in reduced numbers of late-stage B progenitors within bone marrow. While numbers of mature peripheral B and T cells were unaffected, recovery from sub-lethal irradiation or transplantation was dramatically reduced. LPS normally suppresses B precursor expansion in response to interleukin 7, but STAP-2 deficiency made them more resistant. Preliminary RNA-Seq analyses indicate many signaling pathways in B progenitors are STAP-2 dependent. These findings suggest STAP-2 modulates formation of B lymphocytes in demand conditions. Further study of this adapter protein could suggest ways to speed recovery of humoral immunity following chemotherapy or transplantation.

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Signal-transducing adaptor protein-2 delays recovery of B lineage lymphocytes during hematopoietic stress.

Project description:Signal-transducing adaptor protein-2 (STAP-2) was discovered as a C-FMS/M-CSFR interacting protein and subsequently found to function as an adaptor of signaling or transcription factors. These include STAT5, MyD88 and IκB kinase in macrophages, mast cells, and T cells. There is additional information about roles for STAP-2 in several types of malignant diseases including chronic myeloid leukemia, however, none have been reported concerning B lineage lymphocytes. We have now exploited gene targeted and transgenic mice to address this lack of knowledge, and demonstrated that STAP-2 is not required under normal, steady-state conditions. However, recovery of B cells following transplantation was augmented in the absence of STAP-2. This appeared to be restricted to cells of B cell lineage with myeloid rebound noted as unremarkable. Furthermore, all hematological parameters were observed to be normal once recovery from transplantation was complete. Furthermore, overexpression of STAP-2, specifically in lymphoid cells, resulted in reduced numbers of late-stage B cell progenitors within the bone marrow. While numbers of mature peripheral B and T cells were unaffected, recovery from sub-lethal irradiation or transplantation was dramatically reduced. Lipopolysaccharide (LPS) normally suppresses B precursor expansion in response to interleukin 7, however, STAP-2 deficiency made these cells more resistant. Preliminary RNA-Seq analyses indicated multiple signaling pathways in B progenitors as STAP-2-dependent. These findings suggest that STAP-2 modulates formation of B lymphocytes in demand conditions. Further study of this adapter protein could reveal ways to speed recovery of humoral immunity following chemotherapy or transplantation.

| S-EPMC7849758 | biostudies-literature

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