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We present the volumetric rates and luminosity functions (LFs) of Type Ia supernovae (SNe Ia) from the V -band All-Sky Automated Survey for Supernovae (ASAS-SN) catalogues spanning discovery dates from UTC 2014 January 26 to UTC 2017 December 29. Our standard sample consists of 404 SNe Ia with |$m_{\mathrm{{\it V},peak}} \lt 17\, \mathrm{mag}$| and Galactic latitude | b | > 15°. Our results are both statistically more precise and systematically more robust than previous studies due to the large sample size and high spectroscopic completeness. We make completeness corrections based on both the apparent and absolute magnitudes by simulating the detection of SNe Ia in ASAS-SN light curves. We find a total volumetric rate for all subtypes of |$R_{\mathrm{tot}} = 2.28^{+0.20}_{-0.20} \times 10^{4}\, \mathrm{yr}^{-1}\, \mathrm{Gpc}^{-3}\, h^{3}_{70}$| for |$M_{\mathrm{{\it V},peak}} \lt -16.5\, \mathrm{mag}$| (⁠|$R_{\mathrm{tot}} = 1.91^{+0.12}_{-0.12} \times 10^{4}\, \mathrm{yr}^{-1}\, \mathrm{Gpc}^{-3}\, h^{3}_{70}$| for |$M_{\mathrm{{\it V},peak}} \lt -17.5\, \mathrm{mag}$|⁠) at the median redshift of our sample, z med = 0.024. This is in agreement (1σ) with the local volumetric rates found by previous studies. We also compile LFs for the entire sample as well as for subtypes of SNe Ia for the first time. The major subtypes with more than one SN include Ia-91bg, Ia-91T, Ia-CSM, and Ia-03fg with total rates of |$R_{\mathrm{Ia-91bg}} = 1.4^{+0.5}_{-0.5} \times 10^{3}\, \mathrm{yr}^{-1}\, \mathrm{Gpc}^{-3}\, h^{3}_{70}$|⁠ , |$R_{\mathrm{Ia-91T}} = 8.5^{+1.6}_{-1.7} \times 10^{2}\, \mathrm{yr}^{-1}\, \mathrm{Gpc}^{-3}\, h^{3}_{70}$|⁠ , |$R_{\mathrm{Ia-CSM}} = 10^{+7}_{-7}\, \mathrm{yr}^{-1}\, \mathrm{Gpc}^{-3}\, h^{3}_{70}$|⁠ , and |$R_{\mathrm{Ia-03fg}} = 30^{+20}_{-20}\, \mathrm{yr}^{-1}\, \mathrm{Gpc}^{-3}\, h^{3}_{70}$|⁠ , respectively. We estimate a mean host extinction of |$E(V-r) \approx 0.2\, \mathrm{mag}$| based on the shift between our V band and the Zwicky Transient Facility r -band LFs. [ABSTRACT FROM AUTHOR]

Th cells recognize protein Ags as short peptides bound to MHC class II molecules. Altered peptide ligands can antagonize (inhibit) T cell responses to stimulatory peptides. Peptides generated by APC may contain peptide flanking residues (PFR), which lie outside the minimal binding epitope and can be recognized by the TCR. Our data show that PFR-dependent T cells were found to be potently antagonized by peptides that lack PFR and responded poorly to native protein or the immunogenic epitope delivered by a recombinant influenza virus. These data provide the first evidence that Ag processing generates both stimulatory and antagonist peptides from a single immunogenic epitope, an observation that may have important implications for T cell immunoregulation and autoimmunity.

Anti-DNA antibodies are a major contributor to the pathogenesis associated with the autoimmune disease systemic lupus erythematosus in mice and human. The accumulation of a large body of structural information on autoimmune anti-DNA antibodies over the past several years, particularly from mice, has provided considerable insight into the structure, function, and biology of this important class of autoantibodies. Even though the germline repertoire of light and heavy chain variable regions that may encode DNA-specific antibodies is very large in mice, there are individual light and heavy chain variable region genes that have been recurrent and preferentially expressed among anti-DNA hybridomas. This has been particularly true for hybridomas producing antibodies that bind duplex, B-form, mammalian DNA (dsDNA). Recurrent somatically derived variable region structures, particularly arginines in the third complementary-determining region of the heavy chain (VH-CDR3), have also been recurrent and preferentially expressed among monoclonal anti-DNA antibodies. In fact specificity for dsDNA can be correlated to the relative amino acid position at which arginines are expressed within VH-CDR3 of anti-DNA. Most important from the results of structural analyses of monoclonal anti-DNA autoantibodies has been the realization that autoimmunity to DNA results from a clonally selective, antigen-specific immune response to DNA. Autoimmune antibodies to DNA have all of the characteristics of secondary immune antibodies. In further support of this hypothesis, we have been able to induce anti-DNA antibodies in normal, nonautoimmune mice by immunization with immunogenic DNA-peptide complexes. The induced antibodies have all of the structural and functional characteristics of autoimmune anti-DNA including the pathogenetic potential to induce glomerulonephritis. This review summarizes the results of research from our laboratory that support the above conclusions.

Important to the immunopathology associated with the autoimmune disease systemic lupus erythematosus, is the production of autoantibody to DNA. Crucial to understanding the immunological basis for autoimmunity to DNA is knowing whether the anti-DNA autoantibody is the product of clonally-selective, antigen-specific B cell stimulation or non-selective, polyclonal B cell activation. Structural analyses of the immunoglobulin variable-regions of both early, IgM and late, IgG anti-DNA antibodies from lupus-prone (NZB x NZW) F1 mice have indicated that both IgM and IgG anti-DNA autoantibodies are generated by clonally-selective B cell stimulation. Within individual autoimmune mice the later appearing, IgG anti-DNA autoantibodies are structurally similar to the earlier appearing, IgM antibodies, and in some cases both IgM and IgG may be produced by the same B cell clones. The variable-region structural data also suggest that DNA or complexes containing DNA may be the immunogenic stimuli for autoantibody to DNA. In support of this conclusion, normal mice immunized with immunogenic peptide-DNA complexes produce anti-DNA antibodies with structural and serological characteristics similar if not identical to those of autoimmune anti-DNA antibodies. Normal mice immunized with peptide-DNA complexes eventually develop immunopathology that resembles lupus nephritis. These results suggest that autoimmunity to DNA and subsequent autoimmune disease in SLE may result from a specific immune response to DNA containing antigens.