In the bone marrow (BM), mesenchymal stromal cell (MSC) niches support the differentiation of haematopoietic cells, lymphoid progenitors and B lymphocytes (LB). While lymphocytes in the periphery reciprocally have the ability to control the development of their supporting niches, this knowledge remains limited in the BM. The main aim of my thesis is to understand the regulatory mechanisms in place between MSC niches and LB progenitors. To achieve this, we have used mouse models with a blockage of early LB differentiation, at the pro-B/pre-B transition (µMT mice), or a complete blockage of lymphoid differentiation (RAG2-/-yc-/- mice = RAGyc mice). Phenotypic analysis of medullary niches by flow cytometry showed an increase in perisinusoidal stromal cells (PSS) in µMT mice, a niche of pro-B cells secreting IL7, correlated with an accumulation of pro-B cells blocked at this stage. This increase in PSS is even greater in the complete absence of lymphoid cells, confirming the capacity of the latter to control the nature of the MSCs in the BM. Recent results show that in an inflammatory situation, mature LB recirculating in the BM can block IL7 secretion by PSS by activating the lymphotoxin pathway, and thus slow down the production of pro-B cells and consequently mature LB. Our results could suggest the existence of a homeostatic control loop of haematopoiesis by mature lymphoid cells. These results will be confirmed by single-cell RNAseq analysis of haematopoietic progenitors and MSCs in order to better understand the interactions and signaling pathways involved. Understanding the molecular dialogue between MSCs and lymphoid cells is relevant in cancerology and will be extended to the study of the establishment of support niches in B-type acute lymphoblastic leukemia, the malignant equivalent of LB differentiation.