In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Example Input: The presentation of viral peptide epitopes to host cytotoxic T lymphocytes (CTLs) is crucial for adaptive cellular immunity to clear the virus infection, especially for some chronic viral infections. Indeed, hosts have developed effective strategies to achieve this goal. The ideal scenario would be that the peptide epitopes stimulate a broad spectrum of CTL responses with diversified T-cell receptor (TCR) usage (the TCR repertoire). It is believed that a diversified TCR repertoire requires a "featured" peptide to be presented by the host major histocompatibility complex (MHC). A featured peptide can be processed and presented in a number of ways. Here, using the X-ray diffraction method, the crystal structures of an antigenic peptide derived from rinderpest virus presented by bovine MHC class I N*01801 (BoLA-A11) have been solved, and two distinct conformations of the presented peptide are clearly displayed. A detailed analysis of the structure and comparative sequences revealed that the polymorphic amino acid isoleucine 73 (Ile73) is extremely flexible, allowing the MHC groove to adopt different conformations to accommodate the rinderpest virus peptide. This makes the peptide more featured by exposing different amino acids for T-cell recognition. The crystal structures also demonstrated that the N*01801 molecule has an unusually large A pocket, resulting in the special conformation of the P1 residue at the N terminus of the peptide. We propose that this strategy of host peptide presentation might be beneficial for creating a diversified TCR repertoire, which is important for a moreeffective CTL response. Viral diseases and other infections caused by intracellular pathogens of cattle result in large global economic losses every year. In the past several decades, rinderpest virus (RPV) (23, 40), foot-and-mouth disease virus (FMDV) (7), and bovine tuberculosis infection (62) have brought disastrous consequences, including social panic and even a threat to human health. Nearly 6 decades ago, most countries were committed to developing more-effective vaccines (46), and remarkable achievements were made in controlling threatening bovine viral infectious diseases and other zoonoses (23, 46). In the 1960s, British virologist Walter Plowright developed a live attenuated vaccine against rinderpest virus, which was widely used in rinderpest eradication efforts (40). However, it still remains extremely challenging for humans to completely eradicate a virus. The questions of how the bovine attenuated vaccine induces immune responses and how the viral peptides are presented and recognized by host immune molecules are still largely unanswered. Therefore, studies on bovine immunity against the rinderpest virus may provide clues for our battle against other viral infections. Generally speaking, effective vaccines have common characteristics: they are rich in T-cell and B-cell epitopes and can induce the immune system to generate protective immune responses (3, 36, 54) . During this process, major histocompatibility complex (MHC) molecules play a pivotal role in the host. MHC class I (MHC I) molecules form a heterotrimer complex composed of the heavy chain of MHC, the antigenic peptide, and ␤ 2 -microglobulin (␤ 2 m). Generally, MHC I loads endogenous peptides, including the virus-derived peptides. Briefly, at the initial stage of virus infection, antigenic proteins are processed in a proteasome-dependent or -independent manner. The resultant short peptides are then transported to the endoplasmic reticulum and are loaded onto the peptidebinding grooves of MHC I molecules. Consequently, the peptide-loading MHC I complexes are translocated to the cell surface and are recognized by cytotoxic T lymphocytes (CTLs) with specific T-cell receptors (TCRs) (49, 63). This immune recognition induces an MHC-restricted CD8 ϩ T-cell response that is characterized by the killing and elimination of the infected cells by effector T cells. The majority of virus-derived peptides are processed and presented through this pathway
Example Output: Two Distinct Conformations of a Rinderpest Virus Epitope Presented by Bovine Major Histocompatibility Complex Class I N*01801: a Host Strategy To Present Featured Peptides ᰔ †

Example Input: The family Potyviridae encompasses~30% of plant viruses and is responsible for significant economic losses worldwide. Recently, a small overlapping coding sequence, termed pipo, was found to be conserved in the genomes of all potyvirids. PIPO is expressed as part of a frameshift protein, P3N-PIPO, which is essential for virus cell-to-cell movement. However, the frameshift expression mechanism has hitherto remained unknown. Here, we demonstrate that transcriptional slippage, specific to the viral RNA polymerase, results in a population of transcripts with an additional "A" inserted within a highly conserved GAAAAAA sequence, thus enabling expression of P3N-PIPO. The slippage efficiency is~2% in Turnip mosaic virus and slippage is inhibited by mutations in the GAAAAAA sequence. While utilization of transcriptional slippage is well known in negative-sense RNA viruses such as Ebola, mumps and measles, to our knowledge this is the first report of its widespread utilization for gene expression in positive-sense RNA viruses.
Example Output: Transcriptional slippage in the positive-sense RNA virus family Potyviridae

Example Input: Tumor necrosis factor receptor-associated factor 3 (TRAF3), a member of the TRAF family of cytoplasmic adaptor proteins with E3 ligase activity, is ubiquitously expressed in various cell types of the immune system. It is shared for signaling by a variety of adaptive and innate immune receptors as well as cytokine receptors. Previous studies examining conditional TRAF3-deficient mouse models that have the Traf3 gene specifically deleted in B lymphocytes or T lymphocytes have revealed the diverse and critical in vivo functions of TRAF3 in adaptive immunity. Although in vitro evidence points to a pivotal and indispensable role for TRAF3 in type I interferon production induced by pattern recognition receptors in macrophages and dendritic cells, the in vivo functions of TRAF3 in the innate immune system had long remained unclear. Three laboratories have recently addressed this gap in knowledge by investigating myeloid cell-specific TRAF3deficient (genotype: TRAF3 flox/flox LysM +/Cre ) mice. The new evidence together demonstrates that specific ablation of TRAF3 in myeloid cells leads to inflammatory diseases, altered progression of diabetes, and spontaneous development of different types of tumors and infections in mice. These new findings indicate that TRAF3 acts as an anti-inflammatory factor and is required for optimal innate immunity in myeloid cells. Strikingly, the new evidence also identifies TRAF3 as a novel tumor suppressor gene in macrophages and other myeloid cells. In this review, we discuss and summarize the new findings and current knowledge about the multi-faceted regulatory roles and complex signaling mechanisms of myeloid cell TRAF3 in inflammation, innate immunity, and tumor development.
Example Output:
TRAF3: a novel tumor suppressor gene in macrophages