Disclosed is means which enables simple and rapid detection of the presence or absence of mismatch repair activity, and which is useful for diagnosis and treatment of mismatch repair-deficient cancers. In an integrated-type nucleic acid construct provided by the present invention, [promoter region], [5′-side region+first homologous region], and [second homologous region+3′-side region] are placed in the same nucleic acid molecule. In a divided-type nucleic acid construct, [promoter region], [5′-side region+first homologous region], and [second homologous region+3′-side region] are placed in two different nucleic acid molecules. The nucleic acid construct of the present invention can be used as a therapeutic agent for mismatch repair-deficient cancer, as a diagnostic agent for mismatch repair-deficient cancer, or as a companion diagnostic agent for predicting an effect of an anticancer drug for mismatch repair-deficient cancer, containing the nucleic acid construct.

Disclosed are methods of identifying immunosuppressive T.sub.R1 regulatory T cells, including in methods of diagnosing the presence of immune tolerance, methods of producing immunosuppressive regulatory T cells, and methods of eliciting immune tolerance in a subject. These methods include screening T cells to detect Eomes.sup.+IL-10.sup.+ T cells or expressing recombinant Eomes in T cell populations to generate immunosuppressive regulatory T cells.

Devices, systems, and methods can be used for the automated production of dendritic cells (DC) from dendritic cell progenitors, such as monocytes obtained from peripheral blood. The invention makes it possible to obtain sufficient quantities of a subject's own DC for use in preparing and characterizing vaccines, for activating and characterizing the activation state of the subject's immune response, and to aid in preventing and/or treating cancer or infectious disease.

Safe, rapid and efficient methods for producing antigen-specific T cells recognizing human papilloma virus or HPV antigens.

To provide extracellular vesicles capable of satisfactorily activating, etc., antigen-specific T cells. Provided are said antigen-presenting extracellular vesicles that present an antigen-presenting MHC molecule and a T-cell-stimulating cytokine extramembranously.

The invention provides a Siniperca chuatsi IL-6 gene and a detection method for a disease-resistant SNP marker. A cDNA sequence of S. chuatsi IL-6 gene is cloned, as shown in SEQ ID NO: 1. A IL-6 gene gDNA sequence containing an intron of the S. chuatsi IL-6 gene is cloned, as shown in SEQ ID NO: 2. A primer for amplifying a disease-resistant SNP locus is designed according to IL-6 gDNA sequence, and S. chuatsi IL-6 gene is amplified to obtain an amplification product which is sequenced, and the SNPs loci relevant to virus disease-resistance are found out and the SNP locus is determined according to DNA peak profile. The IL-6 cDNA full-length sequence and IL-6 gDNA full-length sequence are cloned firstly. The SNP locus relevant to virus disease resistance of S. chuatsi IL-6 gene is detected, thereby providing a new method for breeding of S. chuatsi.

Disclosed are cysteine variants of interleukin-11 (IL-11) and methods of making and using such proteins in therapeutic applications.

Fully human monoclonal Abs includes (i) an antigen-binding variable region that exhibits very high binding affinity for IL-1α and (ii) a constant region that is effective at both activating the complement system though C1q binding and binding to several different Fc receptors.

The present invention relates to polypeptides which are covalently bound to molecular scaffolds such that two or more peptide loops are subtended between attachment points to the scaffold. In particular, the invention describes peptides which are high affinity binders of CD137. The invention also includes drug conjugates comprising said peptides, conjugated to one or more effector and/or functional groups, to pharmaceutical compositions comprising said peptide ligands and drug conjugates and to the use of said peptide ligands and drug conjugates in preventing, suppressing or treating a disease or disorder mediated by CD137.

Mice that comprise a replacement of endogenous mouse IL-6 and/or IL-6 receptor genes are described, and methods for making and using the mice. Mice comprising a replacement at an endogenous IL-6Rα locus of mouse ectodomain-encoding sequence with human ectodomain-encoding sequence is provided. Mice comprising a human IL-6 gene under control of mouse IL-6 regulatory elements is also provided, including mice that have a replacement of mouse IL-6-encoding sequence with human IL-6-encoding sequence at an endogenous mouse IL-6 locus.