A method for screening a therapeutic drug used for treating psoriasis includes the steps of: (a) isolating and separating fresh peripheral blood mononuclear cells (PBMC); (b) activating the peripheral blood mononuclear cells with a stimulant to cause the cells to produce IFN-γ and RANTES; (c) administering the plurality of candidate drugs to the activated peripheral blood mononuclear cells; (d) detecting expression levels of IFN-γ and RANTES in the peripheral blood mononuclear cells administered with the plurality of candidate drugs; (e) recognizing and removing a disqualified drug from the plurality of candidate drugs according to a variation degree of the expression level of RANTES; and (f) screening the therapeutic drug from the plurality of the candidate drugs excluding the disqualified drug according to the expression level of IFN-γ.

Disclosed are methods of isolating a TCR having antigenic specificity for a mutated amino acid sequence encoded by a cancer-specific mutation, the method comprising: identifying one or more genes in the nucleic acid of a cancer cell of a patient, each gene containing a cancer-specific mutation that encodes a mutated amino acid sequence; inducing autologous APCs of the patient to present the mutated amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated amino acid sequence; selecting the autologous T cells; and isolating a nucleotide sequence that encodes the TCR from the selected autologous T cells, wherein the TCR has antigenic specificity for the mutated amino acid sequence encoded by the cancer-specific mutation. Also disclosed are related methods of preparing a population of cells, populations of cells, TCRs, pharmaceutical compositions, and methods of treating or preventing cancer.

The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TH17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.

Disclosed are methods of isolating a TCR having antigenic specificity for a mutated amino acid sequence encoded by a cancer-specific mutation, the method comprising: identifying one or more genes in the nucleic acid of a cancer cell of a patient, each gene containing a cancer-specific mutation that encodes a mutated amino acid sequence; inducing autologous APCs of the patient to present the mutated amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated amino acid sequence; selecting the autologous T cells; and isolating a nucleotide sequence that encodes the TCR from the selected autologous T cells, wherein the TCR has antigenic specificity for the mutated amino acid sequence encoded by the cancer-specific mutation. Also disclosed are related methods of preparing a population of cells, populations of cells, TCRs, pharmaceutical compositions, and methods of treating or preventing cancer.

The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TL17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.

The present invention relates to an aptamer comprising a nucleotide sequence SEQ ID NO: 1, preferably comprising or consisting of a nucleotide sequence SEQ ID NO: 4-6. The invention further relates to a composition comprising the aptamer, and the use of the aptamer as a medicament or a diagnostic reagent, particularly for use in the detection or diagnosing of a rejection of a renal allograft.

The present invention provides a prophylactic agent, onset-suppressing agent, or therapeutic agent for progressive immune demyelinating diseases comprising, as an active ingredient, a substance capable of suppressing or inhibiting production of prolactin.

The present invention relates to the finding that TL1A enhances differentiation of TH17 cells, and enhance IL17 secretion from TL17 cells. In one embodiment, the present invention provides a method of treating an inflammatory disease comprising determining the presence of a TL1A signaling profile, and treating the disease by administering a composition comprising a therapeutically effective dosage of one or more inhibitors of TL1A or TH17 cell differentiation. In another embodiment, the disease is characterized by TH17 differentiation.

The present invention provides a prophylactic agent, onset-suppressing agent, or therapeutic agent for progressive immune demyelinating diseases comprising, as an active ingredient, a substance capable of suppressing or inhibiting production of prolactin.

The invention provides methods and systems for detecting a biomarker related to AIN in a biological sample, and use thereof alone or as part of a diagnostic index for identifying and treating subjects at risk of AIN.