The present invention relates to a method for treating autism spectrum disorder, a mouse for monitoring autism spectrum disorder, and a method for screening a candidate for preventing or treating autism spectrum disorder. Specifically, according to the present invention, the output signal (or excitation of population) of neurons of the ventrolateral thalamus (VL), the laterodorsal thalamus (LD) or the striatum may be suppressed by introducing a halorhodopsin protein into neurons of the ventrolateral thalamus (VL), the laterodorsal thalamus (LD) or the striatum and then irradiating light to induce hyperpolarization of the halorhodopsin protein. Thus, the present invention has the effect of preventing or treating autism.

The present disclosure relates to the genetically modified non-human animals that express a human or chimeric (e.g., humanized) T-cell immunoglobulin and mucin-domain containing-3 (TIM-3), and methods of use thereof.

In one aspect, the invention provides methods of inhibiting the effects of MASP-2-dependent complement activation in a living subject. The methods comprise the step of administering, to a subject in need thereof, an amount of a MASP-2 inhibitory agent effective to inhibit MASP-2-dependent complement activation. In some embodiments, the MASP-2 inhibitory agent inhibits cellular injury associated with MASP-2-mediated alternative complement pathway activation, while leaving the classical (C1q-dependent) pathway component of the immune system intact. In another aspect, the invention provides compositions for inhibiting the effects of lectin-dependent complement activation, comprising a therapeutically effective amount of a MASP-2 inhibitory agent and a pharmaceutically acceptable carrier.

The present invention provides a method for treating wounds by applying cells as described in this application. In one aspect the method provides treatment for cutaneous wounds. In general embodiments the cells are delivered to the wound without being attached to a functionalized substrate in the delivery vehicle.

The invention provides compositions and methods useful for the treatment and prevention of conditions associated with short telomere length.

The skin is one of first lines of defense against external threats. Tissue-resident macrophages have pivotal functions in tissue-barrier integrity and homeostasis. Upon skin inflammation, a functional crosstalk between the sensory nervous system and tissue-resident immune cells can regulate cutaneous immune responses. However, depending on the pathological context, sensory neurons display pro- or anti-inflammatory regulatory properties. Here the inventors identify, in a model of ultraviolet (UV)-induced skin N damage, a regulatory role for type C low-threshold mechanoreceptor (C-LTMR) sensory neurons on the dynamic of dermal macrophage replacement by inflammatory monocytes through the neuropeptide TAFA4. Tafa4-KO mice present an unresolved fibrotic dermis after UV irradiation. Increased fibrotic score correlates with the upstream persistency of inflammatory monocytes and their MHC-II.sup.+ macrophage progeny. Bone marrow chimera revealed that inflammatory monocyte differentiation towards CD206+ dermal macrophage is increased in Tafa4KO recipient. Finally, intradermal injection of TAFA4 at the site of UV irradiation reduces inflammatory monocytes accumulation and skin inflammation in Tafa4-KO mice. The results provide new insight about tissue-resident macrophages dynamic during the resolution of skin fibrosis and thus renders credible the use of TAFA4 for the treatment of skin inflammation.

Non-human animals, cells, methods and compositions for making and using the same are provided, wherein the non-human animals and cells comprise a humanized a proliferation-inducing ligand gene. Non-human animals and cells that express a human or humanized a proliferation-inducing ligand protein from an endogenous a proliferation-inducing ligand locus are described.

Provided are a knockout mouse, a method for screening a substance for suppressing mesial temporal lobe epilepsy, and a method for selecting a technique for suppressing mesial temporal lobe epilepsy. A knockout mouse 30 or more days of age that has lost the function of the Girdin gene in at least the nervous tissues and exhibits the phenotypes of (1), (2), and (3) below. (1) hippocampal sclerosis should be present, (2) extrahippocampal brain damage should be limited, and (3) spontaneous epilepsy that can be said to be of hippocampal origin should be present.

The inventive technology is directed to the generation of a novel transgenic mammalian model for the study of Laing distal myopathy. The novel animal model of the invention may include a transgenic animal, and preferably a transgenic mouse, expressing the β-myosin R1500P mutation transgene that produces one or more phenotypes associated with MPD1. The β-myosin R1500P mutation transgene may further be selectively expressed in fast muscle tissue of the transgenic animal.

The present invention relates to a Crumbs homologue (CRB) therapeutic for use as a medicament or in a method of treatment or prophylaxis, for example in the treatment or prophylaxis of a retinal disorder due to mutations in the Crumbs homologue-1 (CRB1) gene, such as Leber's congenital amaurosis 8 (LCA8) or retinitis pigmentosa 12 (RP12). In particular, the present invention relates to a recombinant viral vector comprising CRB2 or modified non-toxic forms of either CRB1 or CRB3 that resemble CRB2.