As a result of dedicated studies, the present inventors succeeded in discovering, for the first time, that fibrogenesis could be suppressed at the physiological tissue level by inhibiting sulfation at position 4 or 6 of GalNAc, which is a sugar that constitutes sugar chains. Furthermore, the present inventors conducted studies using various disease model animals, and as a result, successfully demonstrated that inhibitors of sulfation at position 4 or 6 of GalNAc had therapeutic effects on diseases caused by tissue fibrogenesis (tissue fibrogenic disorders).

It is provided a method of producing high-quality engineered cartilage graft in a human of animal, such as nasal cartilage graft, comprising expanding chondrocytes and/or chondroprogenitors, e.g. autologous human nasoseptal chondrocytes (hNC,) from a donor patient by selecting expanded chondrocytes and/or chondroprogenitors by detecting the expression of at least one surfaceome protein gene or secretome protein gene, wherein the at least one surfaceome protein gene is ADGRG1, NPR3, SLC16A4, TSPAN13, FZD4 and SLC22A23 and the at least one secretome protein gene is ADGRG1, B3GNT7, COLGALT2, IGFBP3, STC2, SAA1, ANGPLT1, COL8A2, INHBB, ADAMTS9, ORM1, COL14A1, DCN, COL21A1, ENOX1, IL7, MXRA5 GAL, TFRC, SERPINA9, LIF, GDF6 and COL5A3.

Assays for screening for, or determining activity of, an agonist of lymphocyte-activation gene 3 (LAG-3) are described. According to the assays, a plurality of effector T cells is provided, each effector T cell expressing LAG-3 and a T-cell receptor (TCR) on its surface, and comprising a reporter gene encoding a reporter, wherein expression of the reporter is regulated by LAG-3-mediated inhibition of TCR signaling within the effector T cells. Activity of the agonist is determined from the extent to which expression of the reporter is altered in the presence of the agonist compared with expression of the reporter in the absence of the agonist. The assays may be used for determining the potency of a preparation of the agonist as part of a quality control step in production of the agonist, or for stability testing of a preparation of the agonist. Kits for carrying out the assays are also described.

The present disclosure provides a newly-identified transitional cell state in alveolar regeneration, models to ablate lung alveolar type-1 cells that leads to lung fibrosis and emphysema, a scalable, an ex vivo lung fibrosis model that uses co-cultured lung fibroblasts and pre-alveolar type-1 transitional cell state (PATS) for the use of disease modeling and drug screening, and methods of using same.

A method of inducing expression of a calcium channel and/or a calcium pump in a cell includes: irradiating the cell with light in a wavelength range of 315-325 nm. The calcium channel and/or the calcium pump is/are at least one selected from the group consisting of dihydropyridine receptor (DHPR), voltage-gated calcium channel (VGCC), ryanodine receptor (RYR), and sarcoendoplasmic reticulum Ca.sup.2+-ATPase (SERCA).

Provided herein are methods and compositions related to the selection T cells and/or subjects for adoptive immunotherapy based on the expression of one or more biomarkers.

The present technology relates, inter alia, to perturbagens and methods for directing a change in the cell state of a progenitor cell. It also relates to methods for increasing a quantity of beige adipocytes, beige preadipocytes, and/or immediate progenitors thereof and/or the ratios thereof. Further, the present technology relates to methods for treating diseases or disorders characterized by, at least, abnormal numbers, ratios or bodily distributions of beige adipocytes, beige preadipocytes, white adipocytes, white preadipocytes, or immediate progenitors thereof, with respect to each other.

The present invention relates to methods and pharmaceutical composition for the treatment of T-helper type 2 (Th2)-mediated diseases. More particularly, the present invention relates to an inhibitor of the Suv39h1-HP1a silencing pathway for use in the treatment of a T-helper type 2 (Th2)-mediated disease, in particular allergic asthma.

The present invention pertains to: the provision of a method for promoting skin wound healing and a composition to be used for promoting skin wound healing; the provision of a method useful for preventing or ameliorating ulcers and bedsores or a composition therefor; the provision of a method for preventing skin aging and a composition to be used for preventing skin aging; the provision of a composition useful for preventing or ameliorating skin damage caused by an anticancer agent; and, furthermore, the provision of a method for enhancing the regeneration ability of epidermal stem cells and a composition for enhancing the regeneration ability of epidermal stem cells. More specifically, use of a composition, said composition being characterized by comprising, as an active ingredient, a substance selected from the group consisting of a substance which induces or maintains the expression of COL17A1 in cells, a substance which inhibits the degradation of COL17A1 in cells, a substance which promotes the competitive amplification ability of epidermal stem cells, a substance which suppresses genomic stress or oxidative stress in cells and a substance which prevents DNA damage in cells, enables the promotion of skin wound healing, protection from an anticancer agent and prevention of skin aging. Thus, the regeneration ability of epidermal stem cells can be enhanced.

The invention provides methods for treating pathological conditions associated with an undesirable inflammatory component. The invention is generally directed to reducing inflammation by administering cells that modulate microglia activation. The invention is also directed to drug discovery methods to screen for agents that modulate the ability of the cells to modulate microglia activation. The invention is also directed to cell banks that can be used to provide cells for administration to a subject, the banks comprising cells having desired levels of potency to modulate microglia activation.