The present invention provides peptides of general formula (I) and salts thereof, wherein: R.sub.1 and R.sub.2, taken together, form a birradical linker; and R.sub.2′ is hydrogen; or, alternatively, R.sub.1 is selected from hydrogen, —C(═O)—CH.sub.2—NH—C(═O)—(C.sub.1-C.sub.5)alkyl, and —C(═O)—(C.sub.1-C.sub.20)alkyl; one of R.sub.2 and R.sub.2′ is hydrogen and the other is selected from —C(═O)NR.sub.3R.sub.4, and —C(═O)OH; and R.sub.3 and R.sub.4 are same or different and are selected from hydrogen and (C.sub.1-C.sub.10)alkyl. These peptides are highly efficient in binding and inhibiting FoxP3, being efficient in inhibiting and blocking Treg cell functionality, which make them useful in the treatment of cancer. The present invention also provides constructs comprising the peptide of formula (I) as well as combinations comprising the peptide of formula (I), the construct or both. ##STR00001##

The present invention relates to peptides, proteins, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated T-cell peptide epitopes, alone or in combination with other tumor-associated peptides that can for example serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses, or to stimulate T cells ex vivo and transfer into patients. Peptides bound to molecules of the major histocompatibility complex (MHC), or peptides as such, can also be targets of antibodies, soluble T-cell receptors, and other binding molecules.

Aspects of the disclosure relate to compositions and methods for eliciting (or enhancing) anti-repeat-associated non-ATG (RAN) protein antibody expression or production in a subject. Administration of the compositions according to the methods of the present disclosure may in some embodiments result in decreased levels of RAN protein expression and/or aggregation. Such compositions and methods may therefore be useful for the treatment of diseases and disorders known to be associated with RAN proteins.

A method of direct transdifferentiation of somatic cells into other somatic cells may be convenient and still have good reproducibility, excellent production efficiency, and short performed time. Methods for direct transdifferentiation of somatic cells into other somatic cells may include: (a) introducing a GLIS family gene, a mutated GLIS family gene or a gene product thereof into somatic cells; and (b) culturing the gene-introduced somatic cells in a culture medium containing a component that induces differentiation of the somatic cells or precursor cells of the somatic cells into other somatic cells.

The present invention relates to a cord blood plasma-derived exosome or a mimetic thereof and a pharmaceutical use thereof. More particularly, the present invention provides the use of a human cord blood plasma-derived exosome or an exosome mimetic that mimics the proteomic profile of the cord blood plasma-derived exosome for the improvement, prevention or treatment of various autoimmune diseases or wound healing.

Aspects of the disclosure relate to constructs comprising one or more Ca.sub.v3.2 inhibitory polypeptide that blocks Ca.sub.v3.2 T-type calcium channel activity and nociceptive dorsal root ganglion (DRG) neuron excitation. Also provided herein are methods for treating pain in a subject in need thereof. In particular, provided herein are methods comprising administering Ca.sub.v3.2 inhibitory peptide constructs to a dorsal root ganglion of the subject, whereby expression of the Ca.sub.v3.2 inhibitory polypeptides partially or fully inhibits Ca.sub.v3.2 T-type calcium channel activity in the DRG.

Disclosed are a novel therapeutic means effective and practical against cancer, and a novel substance useful as such a therapeutic means. Provided are novel peptides derived from a partial region of HMGN1, HMGN2, HMGN4 or HMGN5, and anti-cancer agents and anti-cancer effect enhancers containing the peptide as an active ingredient. The peptide of the present invention has an anti-tumor effect even independently, and exerts a remarkably excellent anti-tumor effect particularly when used in combination with an immune checkpoint regulator, or an anti-CD4 antibody or antigen-binding fragment thereof.

As disclosed herein, SIRPα is integral to immuno-evasion by many different cancer types as well as cancer resistance to therapies, and reducing SIRPα levels on can bolster antigen acquisition, processing, and presentation, decrease TME immunosuppression and thereby promote tumor-specific T cell activation to eliminate tumors and generate an adaptive immune response consisting of memory T cells, circulating antibodies, and plasma cells, all of which may be specific for neo-antigens in the original cancer. Therefore, disclosed are activated SIRPα.sup.low macrophages that are useful for treating cancers.

Provided are methods of administering a peptide antagonist of CCAAT/enhancer-binding protein beta (C/EBPβ) and methods of treating solid tumors by administering a peptide antagonist of C/EBPβ.

(Objective) An objective of the present invention is to provide therapeutic agents that, in association with stimulation of PDGFRα-positive cells such as bone marrow mesenchymal stem cells, promote their mobilization into blood and accumulation in a damaged tissue, and induce tissue regeneration in a living body.

(Means for solution) Multiple peptides were synthesized, and the migration-promoting activity of each peptide was evaluated. As a result, the present inventors successfully identified multiple peptides that have migration-promoting activity on a PDGFRα-positive bone marrow mesenchymal stem cell line (MSC-1). Further, the present inventors confirmed that the identified peptides also have migration-promoting activity on skin fibroblasts, which are PDGFRα-positive cells.