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.
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Question: To combat the threat of many emerging infectious diseases, DNA immunization offers a unique and powerful approach to the production of high-quality monoclonal antibodies (mAbs) against various pathogens. Compared with traditional protein-based immunization approaches, DNA immunization is efficient for testing novel immunogen designs, does not require the production or purification of proteins from a pathogen or the use of recombinant protein technology and is effective at generating mAbs against conformation-sensitive targets. Although significant progress in the use of DNA immunization to generate mAbs has been made over the last two decades, the literature does not contain an updated summary of this experience. The current review provides a comprehensive analysis of the literature, including our own work, describing the use of DNA immunization to produce highly functional mAbs, in particular, those against emerging infectious diseases. Critical factors such as immunogen design, delivery approach, immunization schedule, use of immune modulators and the role of final boost immunization are discussed in detail.

Answer: DNA immunization as a technology platform for monoclonal antibody induction


Question: The Collaborative Cross (CC) is a multiparent panel of recombinant inbred (RI) mouse strains derived from eight founder laboratory strains. RI panels are popular because of their long-term genetic stability, which enhances reproducibility and integration of data collected across time and conditions. Characterization of their genomes can be a community effort, reducing the burden on individual users. Here we present the genomes of the CC strains using two complementary approaches as a resource to improve power and interpretation of genetic experiments. Our study also provides a cautionary tale regarding the limitations imposed by such basic biological processes as mutation and selection. A distinct advantage of inbred panels is that genotyping only needs to be performed on the panel, not on each individual mouse. The initial CC genome data were haplotype reconstructions based on dense genotyping of the most recent common ancestors (MRCAs) of each strain followed by imputation from the genome sequence of the corresponding founder inbred strain. The MRCA resource captured segregating regions in strains that were not fully inbred, but it had limited resolution in the transition regions between founder haplotypes, and there was uncertainty about founder assignment in regions of limited diversity. Here we report the whole genome sequence of 69 CC strains generated by paired-end short reads at 303 coverage of a single male per strain. Sequencing leads to a substantial improvement in the fine structure and completeness of the genomes of the CC. Both MRCAs and sequenced samples show a significant reduction in the genome-wide haplotype frequencies from two wild-derived strains, CAST/EiJ and PWK/PhJ. In addition, analysis of the evolution of the patterns of heterozygosity indicates that selection against three wild-derived founder strains played a significant role in shaping the genomes of the CC. The sequencing resource provides the first description of tens of thousands of new genetic variants introduced by mutation and drift in the CC genomes. We estimate that new SNP mutations are accumulating in each CC strain at a rate of 2.4 6 0.4 per gigabase per generation. The fixation of new mutations by genetic drift has introduced thousands of new variants into the CC strains. The majority of these mutations are novel compared to currently sequenced laboratory stocks and wild mice, and some are predicted to alter gene function. Approximately one-third of the CC inbred strains have acquired large deletions (.10 kb) many of which overlap known coding genes and functional elements. The sequence of these mice is a critical resource to CC users, increases threefold the number of mouse inbred strain genomes available publicly, and provides insight into the effect of mutation and drift on common resources.

Answer: Genomes of the Mouse Collaborative Cross


Question: infection , an animal model for multiple sclerosis (MS) , axonal injury precedes inflammatory demyelinating lesions , and the distribution of axonal damage present during the early phase of infection corresponds to regions where subsequent demyelination occurs during the chronic phase. We hypothesized that axonal damage recruits inflammatory cells to sites of Wallerian degeneration , leading to demyelination. Three weeks after TMEV infection , axonal degeneration was induced in the posterior funiculus of mice by injecting the toxic lectin Ricinus communis agglutinin (RCA) I into the sciatic nerve. Neuropathology was examined 1 week after lectin injection. Control mice , infected with TMEV but receiving no RCA I , had inflammatory demyelinating lesions in the anterior/lateral funiculi. Other control mice that received RCA I alone did not develop inflammatory lesions. In contrast, RCA I injection into TMEV-infected mice induced lesions in the posterior funiculus in addition to the anterior/lateral funiculi. We found no differences in lymphoproliferative responses or antibody titers against TMEV among the groups. This suggests that axonal degeneration contributes to the recruitment of inflammatory cells into the central nervous system by altering the local microenvironment. In this scenario, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model). Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). 1 Although its etiology is unknown, epidemiological data and clinical reports support the association of MS with environmental factors, particularly viral infection. In recent years, pathological and neuroimaging studies have re-emphasized the importance of axonal damage in MS. 2 Immunostaining studies have provided direct evidence for axonal damage using antibodies against two markers of injured axons: nonphosphorylated neurofilament protein (NFP) 3 and amyloid precursor protein. 4 Several groups have demonstrated that axonal damage occurred early during the course of MS and that damaged axons were found not only in active demyelinating lesions but also in periplaque white matter without demyelination, 5 remyelinating lesions and normal-appearing white matter. 6,7 Magnetic resonance spectroscopy analyses have also demonstrated gray matter lesions 8 and axonal injury in normal-appearing white matter in MS patients. 7, 9, 10 Axonal damage in normal-appearing white matter has also been found in an animal model for MS, coronavirus-induced demyelination. 11 Although axonal damage in MS is believed to occur secondarily after the destruction of the myelin sheath or oligodendrocytes, the myelin-forming cells, these findings suggest that axonal damage could be independent of demyelinating activity. 12 Wallerian degeneration is the anterograde degeneration of axons caused by injury to the proximal part of the axon or by death of the neuronal cell body. 13 In most cases, the demonstration of Wallerian degeneration in humans has been limited to compact neuronal tracts, such as the corticospinal tract and optic radiation. In MS, Wallerian degeneration was believed to be rare; this was probably attributable to a difficulty in detection because MS lesions are usually not confined to a single pathway or tract. However, more recently, magnetic resonance imaging, 14 -17 magnetic resonance spectroscopy, 18 and autopsy 19 studies have documented the presence of Wallerian degeneration in some patients with MS.

Answer:
Immunopathology and Infectious Disease Targeting Inflammatory Demyelinating Lesions to Sites of Wallerian Degeneration