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.

Q: We investigated the ability of monoclonal B cells to restore primary and secondary T-cell dependent antibody responses in adoptive immune-deficient hosts. Priming induced B cell activation and expansion, AID expression, antibody production and the generation of IgM + IgGand IgM -IgG + antigen-experienced B-cell subsets that persisted in the lymphopenic environment by cell division. Upon secondary transfer and recall the IgM -IgG + cells responded by the production of antigen-specific IgG while the IgM + memory cells secreted mainly IgM and little IgG, but generated new B cells expressing germinal center markers. The recall responses were more efficient if the antigenic boost was delayed suggesting that a period of adaptation is necessary before the transferred cells are able to respond. Overall these findings indicate that reconstitution of a functional and complete memory pool requires transfer of all different antigen-experienced B cell subsets. We also found that the size of the memory B cell pool did not rely on the number of the responding naïve B cells, suggesting autonomous homeostatic controls for naïve and memory B cells. By reconstituting a stable memory B cell pool in immune-deficient hosts using a monoclonal high-affinity B cell population we demonstrate the potential value of B cell adoptive immunotherapy.

A: Regulation and Maintenance of an Adoptive T-Cell Dependent Memory B Cell Pool
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Q: Ten strains of avian infectious bronchitis virus (IBV) were titrated as plaqueforming units in primary chick embryo fibroblast cells. In the absence of trypsin, plaques were only formed by Beaudette-42 and Iowa-609 strains. When trypsin was incorporated in the overlay medium of cell monolayers, all the IBV strains tested produced plaques within 4days after inoculation. Incorporation of 20--40 ~xg of trypsin per ml of the overlay medium seemed to be suitable for plaque formation of IBV. A preliminary investigation was made of the mode of action of trypsin.

A: Archives of Virology Plaque Formation by Avian Infectious Bronehitis Virus in Primary Chick Embryo Fibroblast Cells in the Presence of Trypsin
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Q: Host resistance to viral infection requires type I (a/b) and II (g) interferon (IFN) production. Another important defense mechanism is the degradative activity of macroautophagy (herein autophagy), mediated by the coordinated action of evolutionarily conserved autophagy proteins (Atg). We show that the Atg5-Atg12/Atg16L1 protein complex, whose prior known function is in autophagosome formation, is required for IFNg-mediated host defense against murine norovirus (MNV) infection. Importantly, the direct antiviral activity of IFNg against MNV in macrophages required Atg5-Atg12, Atg7, and Atg16L1, but not induction of autophagy, the degradative activity of lysosomal proteases, fusion of autophagosomes and lysosomes, or the Atg8-processing protein Atg4B. IFNg, via Atg5-Atg12/Atg16L1, inhibited formation of the membranous cytoplasmic MNV replication complex, where Atg16L1 localized. Thus, the Atg5-Atg12/Atg16L1 complex performs a pivotal, nondegradative role in IFNg-mediated antiviral defense, establishing that multicellular organisms have evolved to use portions of the autophagy pathway machinery in a cassette-like fashion for host defense.

A:
Article Nondegradative Role of Atg5-Atg12/ Atg16L1 Autophagy Protein Complex in Antiviral Activity of Interferon Gamma
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