Felipe Andrade's research while affiliated with Johns Hopkins University and other places

... For example, based on spectral counts, the extent of citrullination of R 1303 of myosin heavy chain was higher in the ischemic heart disease group compared with control or idiopathic dilated cardiomyopathy, while citrullination of R 1176 and R 1434 was detected only in control samples. This study thus confirmed in situ citrullination within the myocardium, and the finding of an altered pattern of citrullinated residues in cardiomyopathy suggests that citrullination could play a functional role in myocardial dysfunction [15]. ...

... There is a growing body of studies focusing on the identification of novel autoantibodies and the definition of their clinical implications, such as antiplatelet-derived growth factor receptor (PDGFR), antiangiotensin receptor type 1, antigephyrin and antieukaryotic initiation factor 2B antibodies. [9][10][11][12][13][14] Mechanistically, single-cell analysis reveals broad differences in cell cluster gene expression profiles, showing distinctions in clinical phenotypes and distinct skin score trajectories across autoantibody subgroups of diffuse cutaneous SSc (dcSSc). 15 However, further investigation is required to elucidate the precise pathomechanism of autoantibodies in SSc. ...

... Anti-dsDNA Abs correlate with disease flares, hypocomplementemia, and lupus nephritis and encompass a heterogenous pool of autoantibodies with distinct physicochemical properties. Autoantibodies which crossreact with ds-DNA and other self-antigens and are among the most pathogenic, and include those that also recognize a-actinin to mediate lupus nephritis (5,6), those that cross react with the N-methyl-D-aspartic acid receptor to increase risk of lupus neuropsychosis (7), and those that neutralize DNASE1L3 and are found in patients presenting with higher disease activity scores (8). ...

... We think that in addition to anti-C1q, anti-dsDNA, anti-Smith (anti-Sm), anti-Ro/SSA, anti-La/SSB, anti-ribonucleoprotein (anti-RNP), antiphospholipid antibodies, and complement fractions should be included in the panel of autoantibodies that any patients with suspected of LN should tested at baseline. Recently, anti-alfa enolase (ENO1), anti-histone 2 IgG2, antibodies directed against superoxide dismutase 2 (SOD2), anti-chromatin, anti-nucleosome and ribosomal P emerged in experimental studies, as possible biomarkers of active lupus nephritis, but are not yet available in the clinical setting (58,59,63). Considering the healthcare expenditure of testing the entire panel of available antibodies, complete screening should be performed at SLE diagnosis, while only anti-dsDNA, anti-C1q, and complement fractions should be tested to monitor LN during follow-up. ...

... Except for antibodies to Ro52, antibodies to dsDNA, ribonucleoprotein (RNP), Sm, and DNase1L3 were significantly associated with increased activity levels of IFN-I ( Figure 3E). Interestingly, however, antibodies against Ro52Ex4 and Ro52g-two recently described subsets of anti-Ro52 antibodies 45 -were linked to increased levels of IFN-I and IFN-II, respectively (Figure 3E). No autoantibody was associated with increased IFN-III activity ( Figure 3E). ...

... Regarding the adaptive immune system, autoreactive T cells can escape the process of thymus education in which they are eliminated before accessing the periphery (areas outside the primary lymphoid organs) [5], where they might cross-recognize microbial products or other danger signals. These products can mimic autoantigens, acting as neoantigens that can lead the adaptive immune cells to trigger unintended autoreactive responses [6]. Additionally, failure in the generation and/or function of regulatory T (T reg ) cells and regulatory B (B reg ) cells, key in the development of immunologic tolerance (Box 1), may also be involved in the induction of autoimmune responses [7]. ...

... While the exact cause of RA is unknown, one hypothesis is that polyclonal CD8+ T-cell expansion targeting neutrophils leads to downstream cytotoxic granule release. This induces leukotoxic hypercitrullination, resulting in neoepitope formation secondary to cell lysis [89]. Sixty percent of those with RA have been found to have polymorphisms in HLA-DRB1 with a shared epitope in the hypervariable region of DRB1, leading to poor T cell antigen presentation, along with a smaller subset who present with epigenetic changes, such as PTPN11 hypermethylation, promoting the overexpression of fibroblast-like synoviocytes [90]. ...

... There is growing evidence that COVID-19 can trigger autoimmune responses [89][90][91][92][93][94][95][96][97] that may exacerbate or prolong mitochondrial dysfunction [98]. The immune system's response to SARS-CoV-2 might include the development of autoantibodies that mistakenly target mitochondrial proteins, a phenomenon possibly driven by molecular mimicry [99]. ...

... Previous studies reported the presence of anti-ORF1p antibodies in patients with systemic lupus erythematosus (SLE) 50 . Here we analyzed a set of 17 samples from patients with SLE and found elevated anti-ORF1p (but not anti-ORF2p) IgG titers compared to healthy individuals (median titer, 718 [IQR, 623-1268] vs. 160 [IQR, 75-347]; p<0.0001) (Fig. S11A-B). ...

... The basis of the heterogeneity and cross-reactivity of anti-dsDNA antibodies, however, remains unknown. DNase1L3 is a member of the DNase1 family of DNA endonucleases, which was recently found to be the target of autoantibodies in SLE 20,21 . The enzyme is primarily secreted by myeloid cells (i.e. ...