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: Many factors influence the choice of methods used to develop antibody to infectious agents. In this paper, we review the current status of the main technologies used to produce monoclonal antibodies (mAbs) from the B cells of antigen-sensitized animals. While companies are adopting advanced high-throughput methods, the major technologies used by veterinary and medical research laboratories are classical hybridoma fusion and recombinant library selection techniques. These methods have inherent advantages and limitations but have many common aspects when using immunized rodents. Laboratories with expertise in both methods of antibody development have a distinct advantage in their ability to advance mAb technology. New and re-emerging infectious threats in todayÕs world emphasize the need for quality immunoreagents and the need to maintain expertise in mAb development. We provide examples of some common applications for mAb reagents used to identify pathogens such as the SARS-coronavirus (SARS-CoV), Bacillus anthracis, and foot-and-mouth disease (FMD) virus. We also outline a framework for investigators to make rational decisions concerning which method to use to develop mAbs based upon characteristics of the pathogen under study and the intended downstream application. Lastly, we provide parameters for the immunisation of mice and a classification system which describes the expected outcome for mAb development strategies when using classes of immunogens to generate mAbs with desired activities. Crown Abbreviations: mAb; monoclonal antibody; SARS-CoV; severe acute respiratory syndrome coronavirus; FMD virus; foot-and-mouth disease virus; PA; protective antigen of Bacillus anthracis; BSA; bovine serum albumin; FBS; fetal bovine serum; HAT; hypoxanthine-aminopterin-thymidine; scFv; single chain variable fragment; Fab; fragment responsible for antigen binding; PBL; peripheral blood leucocytes; VP-1; viral protein 1 or 1D viral protein of FMD virus; IEM; immuno-electron microscopy; IHC; immunohistochemistry; IFA; immunoflourescence; V-genes; immunoglobulin variable region genes, responsible for encoding the antigen contact domains. *
Example Output: Rational monoclonal antibody development to emerging pathogens, biothreat agents and agents of foreign animal disease: The antigen scale

Example Input: In this study, the performance of 10 serological assays for the diagnosis of Mycoplasma pneumoniae infection was evaluated. A total of 145 sera from 120 patients were tested. They were obtained from patients who were serologically positive for M. pneumoniae infection as well as from patients who were infected with microorganisms that may cause interstitial pneumonia. The following assays were utilized: SeroMP IgM and IgG, SeroMP recombinant IgM, IgA and IgG, Liaison M. pneumoniae IgM and IgG and M. pneumoniae IgM, IgA and IgG ELISA Medac. The SeroMP Recombinant and Liaison assays both showed low IgM specificity, and crossreactivity was mainly observed in groups of patients with acute cytomegalovirus and Epstein-Barr virus infections. For IgA, the Medac assay was less specific than the SeroMP Recombinant assay. Discrepancies between the four tests were observed in IgG analyses, and due to the lack of a gold standard, 22 results were removed prior to determining the sensitivity and specificity. Therefore, the overall performance of IgG assays may be overstated; nevertheless, the SeroMP assay demonstrated a lack of sensitivity. The seroprevalence of IgG appears to be very low, raising concerns regarding whether the serological techniques can detect IgG levels over time. Serology remains a biological tool of choice for diagnosing M. pneumoniae infection, but improvement and standardization of the assays are needed, particularly for the determination of IgG.
Example Output: Evaluation of 10 serological assays for diagnosing Mycoplasma pneumoniae infection ☆

Example Input: publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. Effector CD8 + T cell-derived interleukin-10 enhances acute liver immunopathology Highlights Effector CD8 + T cells produce IL-10 upon hepatocellular antigen encounter. IL-10 enhances IL-2 responsiveness. IL-10 inhibits antigen-induced effector CD8 + T cell apoptosis. CD8 + T cell-derived IL-10 supports liver immunopathology. Interleukin-10 is mostly regarded as an immunosuppressive cytokine. We show here that HBV-specific CD8 + T cells produce IL-10 upon antigen recognition and that this cytokine enhances CD8 + T cell survival. As such, IL-10 paradoxically promotes rather than suppresses liver disease. Background & Aims: Besides secreting pro-inflammatory cytokines, chemokines and effector molecules, effector CD8 + T cells that arise upon acute infection with certain viruses have been shown to produce the regulatory cytokine interleukin (IL)-10 and, therefore, contain immunopathology. Whether the same occurs during acute hepatitis B virus (HBV) infection and role that IL-10 might play in liver disease is currently unknown. Methods: Mouse models of acute HBV pathogenesis, as well as chimpanzees and patients acutely infected with HBV, were used to analyse the role of CD8 + T cell-derived IL-10 in liver immunopathology. Results: Mouse HBV-specific effector CD8 + T cells produce significant amounts of IL-10 upon in vivo antigen encounter. This is corroborated by longitudinal data in a chimpanzee acutely infected with HBV, where serum IL-10 was readily detectable and correlated with intrahepatic CD8 + T cell infiltration and liver disease severity. Unexpectedly, mouse and human CD8 + T cellderived IL-10 was found to act in an autocrine/paracrine fashion to enhance IL-2 responsiveness, thus preventing antigen-induced HBV-specific effector CD8 + T cell apoptosis. Accordingly, the use of mouse models of HBV pathogenesis revealed that the IL-10 produced by effector CD8 + T cells promoted their own intrahepatic survival and, thus supported, rather than suppressed liver immunopathology. Conclusion: Effector CD8 + T cell-derived IL-10 enhances acute liver immunopathology. Altogether, these results extend our understanding of the cell-and tissue-specific role that IL-10 exerts in immune regulation. Lay summary: Interleukin-10 is mostly regarded as an immunosuppressive cytokine. We show here that HBV-specific CD8 + T cells produce IL-10 upon antigen recognition and that this cytokine enhances CD8 + T cell survival. As such, IL-10 paradoxically promotes rather than suppresses liver disease. Ó
Example Output:
Effector CD8 + T cell-derived interleukin-10 enhances acute liver immunopathology