In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".

Example Input: Abstract: Regulatory T (Treg) cells, whose differentiation and function are controlled by X chromosome-encoded transcription factor Foxp3, are generated in the thymus (tTreg) and extrathymically (peripheral, pTreg), and their deficiency results in fatal autoimmunity. Here, we demonstrate that a Foxp3 enhancer, conserved noncoding sequence 1 (CNS1), essential for pTreg but dispensable for tTreg cell generation, is present only in placental mammals. CNS1 is largely composed of mammalian-wide interspersed repeats (MIR) that have undergone retrotransposition during early mammalian radiation. During pregnancy, pTreg cells specific to a model paternal alloantigen were generated in a CNS1-dependent manner and accumulated in the placenta. Furthermore, when mated with allogeneic, but not syngeneic, males, CNS1-deficient females showed increased fetal resorption accompanied by increased immune cell infiltration and defective remodeling of spiral arteries. Our results suggest that, during evolution, a CNS1-dependent mechanism of extrathymic differentiation of Treg cells emerged in placental animals to enforce maternal-fetal tolerance.. Title: Th2-mediated host protective immunity to intestinal nematode infections.
Example Output: no

Example Input: Abstract: V domain-containing Ig suppressor of T-cell activation (VISTA) is a negative checkpoint regulator that suppresses T cell-mediated immune responses. Previous studies using a VISTA-neutralizing monoclonal antibody show that VISTA blockade enhances T-cell activation. The current study describes a comprehensive characterization of mice in which the gene for VISTA has been deleted. Despite the apparent normal hematopoietic development in young mice, VISTA genetic deficiency leads to a gradual accumulation of spontaneously activated T cells, accompanied by the production of a spectrum of inflammatory cytokines and chemokines. Enhanced T-cell responsiveness was also observed upon immunization with neoantigen. Despite the presence of multiorgan chronic inflammation, aged VISTA-deficient mice did not develop systemic or organ-specific autoimmune disease. Interbreeding of the VISTA-deficient mice with 2D2 T-cell receptor transgenic mice, which are predisposed to the development of experimental autoimmune encephalomyelitis, drastically enhanced disease incidence and intensity. Disease development is correlated with the increase in the activation of encephalitogenic T cells in the periphery and enhanced infiltration into the CNS. Taken together, our data suggest that VISTA is a negative checkpoint regulator whose loss of function lowers the threshold for T-cell activation, allowing for an enhanced proinflammatory phenotype and an increase in the frequency and intensity of autoimmunity under susceptible conditions.. Title: Disruption of the immune-checkpoint VISTA gene imparts a proinflammatory phenotype with predisposition to the development of autoimmunity.
Example Output: yes

Example Input: Abstract: Glucagon is a 29-amino acid pancreatic hormone which counteracts the blood glucose-lowering action of insulin by stimulating hepatic glycogenolysis and gluconeogenesis1. The structure of the hamster pancreatic glucagon precursor has recently been determined from the sequence of a cloned cDNA2. Hamster preproglucagon is a 180-amino acid protein which contains five functional regions; a signal or pre-peptide, an NH2-terminal peptide (also called glicentin-related pancreatic peptide, GRPP), glucagon, and two carboxy-terminal glucagon-like peptides (GLP-1 and GLP-2). The sequences of two non-allelic anglerfish pancreatic glucagon precursors35 have also been determined and their organization is similar but not identical to the hamster protein; they lack the polypeptide segment corresponding to hamster GLP-2. The presence of three regions possessing internal homology, that is, glucagon, GLP-1 and GLP-2, within proglucagon, and the absence of GLP-2 in the anglerfish precursors suggests that the structure of the preproglucagon gene might provide insight into the evolution of this polyprotein. We have isolated and sequenced the human preproglucagon gene and report here that the organization of the human precursor deduced from this sequence is identical to the hamster protein. The gene contains at least three intervening sequences which divide the protein-coding portion of the gene into four regions corresponding to the signal peptide and part of the NH2-terminal peptide, the remainder of the NH2-terminal peptide and glucagon, GLP-1, and GLP-2. The data suggest that triplication and subsequent sequence divergence of an exon encoding glucagon or a glucagon-like peptide produced this polyprotein precursor.. Title: Recurrent venous thromboembolism and bleeding complications during anticoagulant treatment in patients with cancer and venous thrombosis.
Example Output:
no