One aspect of the present disclosure can include a priming medium for creating an isolated population of stem cells having an anti-inflammatory phenotype from an unprimed population of stem cells. The priming media can include a serum-free medium, a functional activator of a Type I interferon (IFN) pathway and a Type II IFN pathway, and at least two pro-inflammatory cytokines. The functional activator and the at least two pro-inflammatory cytokines can be present in an amount sufficient to promote induction of stem cells having an anti-inflammatory phenotype. The cells having an anti-inflammatory phenotype can be marked by increased expression and/or secretion of one or more anti-inflammatory or immune modulatory mediators as compared to the unprimed population of stem cells. Other aspects of the present disclosure can include stem cells made according to the present disclosure as well as therapeutic compositions and uses of the stem cells.

In some aspects, disclosed herein are methods and compositions for treatment or prevention of cerebral palsy using fibroblasts or derivatives thereof. Disclosed herein are fibroblasts and derivatives thereof capable of inducing neurogenesis and/or reducing inflammation in a subject. In some cases, the disclosed methods comprise use of conditioned fibroblasts. Fibroblasts may be conditioned with agents capable of enhancing therapeutic efficacy, for example oxytocin and/or human chorionic gonadotrophin (hCG).

The disclosure provides methods and compositions for affecting the development of antigen presenting cell (APC, e.g., a macrophage or dendritic cell). The methods include maturing an APC, promoting anti-inflammatory phenotype, promoting development of a T regulatory cell (Treg) from a naive T cell. The methods generally include exposing an APC to a tryptophan derived microbiota metabolite (TDMM), such as an anti-inflammatory or pro-mucosal TDMM, and permitting the APC to mature. In some embodiments, the conditioned APC is exposed to a naive T cell to further promote development of a T regulatory cell (Treg). In some embodiments, the TDMM is selected from the group consisting of indole, indole-3-acetate, 5-hydroxyindole, and indole-3-pyruvate.

Provided are methods of in vitro maturation of spermatogonium by culturing the spermatogonium in a three-dimensional methylcellulose culture system (MCS) in a culture medium which comprises an effective concentration of a factor selected from the group consisting of granulocyte macrophages-colony stimulating factor (GM-CSF), interleukin-1 alpha (IL-1alpha), interleukin-1 beta (IL-1beta) and interleukin-6 (IL-6), under conditions capable of differentiating the spermatogonium into at least meiotic and/or postmeiotic cells, thereby in vitro maturing the spermatogonium.

The present invention provides methods of expanding γδ T cells from a non-haematopoietic tissue source. Further provided are compositions of expanded γδ T cells and methods of using the expanded γδ T cells (e.g., apart of an adoptive T cell therapy).

Provided are method for generating αβ T cells from induced pluripotent stem cells. Also provided are genetically engineered iPSCs, αβ T cells, CAR-αβ T cells, and methods of using the same.

A method for screening for target cells, a corresponding test kit and a use thereof, a method for screening cells, and a biological culture chip and a preparation method therefor and a use thereof. The method for screening target cells comprises: culturing said candidate single cells within a culture chamber provided with a signal screening layer, the signal screening layer comprising signal molecules for specific recognition of target molecules; on the basis of signals of the signal molecules, selecting target cells suitable for secreting the target molecules. The method for screening cells comprises: arranging candidate cells in a culture chamber to form target antibody-antigen-signal antibody complexes; on the basis of signals of signal molecules connected to the signal antibodies, determining whether the candidate cells are target cells. The biological culture chip comprises a matrix (100), and a biological culture space arranged on the surface of the matrix (100) and used for culturing biological cells.

The disclosure encompasses the use of fibroblasts and products derived from fibroblasts for treatment of at least frontotemporal dementia. In particular embodiments, the disclosure teaches administration of cells intravenously, intrathecal or intracerebrally in order to reduce inflammation, enhance neurorgeneration and prevent neuronal dysfunction associated with progranulin abnormalities which characterize frontotemporal dementia. In particular embodiments, the disclosure teaches the utilization of exosomes, or apoptotic bodies derived from fibroblasts. In particular embodiments, the disclosure provides the use of genetically modified fibroblasts in order to augment therapy frontotemporal dementia.

A composition for deriving the maturation of dendritic cells includes complex cytokines generated by the simulation, the expression of which is induced on EBV-infected B cells. The dendritic cell maturation process, which conventionally takes approximately 7 days, can be shortened to 2 days, thereby producing dendritic cells in a more economically advantageous and effective manner.

Innate lymphoid cells (ILCs) represent innate versions of T helper and cytotoxic T cells that differentiate from committed ILC precursors (ILCP). Still, how ILCP relate to mature tissue-resident ILCs remains unclear. ILCP that are present in the blood and all tested lymphoid and non-lymphoid human tissues were identified. Human ILCP fail to express the signature transcription factors (TF) and cytokine outputs of mature NK cells and ILCs but are epigenetically poised to do so. Human ILCP robustly generate all ILC subsets in vitro and in vivo. While human ILCP express RAR related orphan receptor C (RORC), circulating ILCP can be found in RORC-deficient patients that retain potential for EOMES.sup.+ NK cells, T-BET.sup.+ ILC1, GATA-3.sup.+ ILC2 and for IL-22.sup.+ but not for IL-17A.sup.+ ILC3. A model of tissue ILC differentiation (‘ILC-poiesis’) is proposed whereby diverse ILC subsets are generated in situ from ILCP in response to environmental stressors, inflammation and infection.