scholarly journals Do COVID-19 RNA-based vaccines put at risk of immune-mediated diseases? In reply to “potential antigenic cross-reactivity between SARS-CoV-2 and human tissue with a possible link to an increase in autoimmune diseases”

2021 ◽  
Vol 224 ◽  
pp. 108665
Author(s):  
Rossella Talotta
Keyword(s):  
At Risk ◽  
Autoimmune Diseases ◽  
Human Tissue ◽  
Cross Reactivity ◽  
Immune Mediated

scholarly journals Reaction of Human Monoclonal Antibodies to SARS-CoV-2 Proteins With Tissue Antigens: Implications for Autoimmune Diseases

2021 ◽  
Vol 11 ◽  
Author(s):  
Aristo Vojdani ◽  
Elroy Vojdani ◽  
Datis Kharrazian
Keyword(s):  
Monoclonal Antibodies ◽  
Autoimmune Diseases ◽  
Human Tissue ◽  
Molecular Mimicry ◽  
Disease Process ◽  
Cross Reactivity ◽  
Immune Reactivity ◽  
Human Tissues ◽  
Human Monoclonal Antibodies ◽  
Tissue Antigens

We sought to determine whether immune reactivity occurs between anti-SARS-CoV-2 protein antibodies and human tissue antigens, and whether molecular mimicry between COVID-19 viral proteins and human tissues could be the cause. We applied both human monoclonal anti-SARS-Cov-2 antibodies (spike protein, nucleoprotein) and rabbit polyclonal anti-SARS-Cov-2 antibodies (envelope protein, membrane protein) to 55 different tissue antigens. We found that SARS-CoV-2 antibodies had reactions with 28 out of 55 tissue antigens, representing a diversity of tissue groups that included barrier proteins, gastrointestinal, thyroid and neural tissues, and more. We also did selective epitope mapping using BLAST and showed similarities and homology between spike, nucleoprotein, and many other SARS-CoV-2 proteins with the human tissue antigens mitochondria M2, F-actin and TPO. This extensive immune cross-reactivity between SARS-CoV-2 antibodies and different antigen groups may play a role in the multi-system disease process of COVID-19, influence the severity of the disease, precipitate the onset of autoimmunity in susceptible subgroups, and potentially exacerbate autoimmunity in subjects that have pre-existing autoimmune diseases. Very recently, human monoclonal antibodies were approved for use on patients with COVID-19. The human monoclonal antibodies used in this study are almost identical with these approved antibodies. Thus, our results can establish the potential risk for autoimmunity and multi-system disorders with COVID-19 that may come from cross-reactivity between our own human tissues and this dreaded virus, and thus ensure that the badly-needed vaccines and treatments being developed for it are truly safe to use against this disease.

scholarly journals Cross—reactivity of antibodies against microbial proteins to human tissues as basis of Crohn’s disease and other autoimmune diseases

2017 ◽  
Author(s):  
Peilin Zhang ◽  
Lawrence M. Minardi ◽  
J. Todd Kuenstner ◽  
Stephen M. Zekan ◽  
Feng Zhu ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Autoimmune Disease ◽  
Crohn's Disease ◽  
Autoimmune Diseases ◽  
Human Tissue ◽  
Mycobacterium Avium Subspecies Paratuberculosis ◽  
Elongation Factor ◽  
Cross Reactivity ◽  
Human Tissues ◽  
Normal Human

AbstractBackgroundAutoimmune disease is generally a systemic inflammatory response with production of autoantibodies. In this study, we investigated the anti-microbial antibodies in circulation in cases of Crohn’s disease (CD), Sjogren’s syndrome (SS) and other autoimmune disease and their roles in the pathogenesis of these autoimmune diseases.Material and methodsWestern blot was used to determine the reactivity of human plasmas from patients with CD and SS as the primary antibodies against the whole microbial extracts. The microbial proteins reactive to patients’ plasma were further identified and the modified sandwich ELISA assays were used to determine the blood levels of antibodies against these microbial proteins in patients with CD and SS. Antibodies against the microbial proteins are used for immunohistochemical staining of normal human tissue.ResultsA group of 7 microbial proteins was identified reactive to the plasmas of patients with CD and SS including DNA-directed RNA polymerase B (RPOB), and elongation factor G (EF-G) fromStaphylococcus aureusandStaphylococcus pseudintermedius(S. aureusandS. pseudintermedius), ATP synthase alpha (ATP5a) and heat shock protein 65 (Hsp65) fromMycobacterium avium subspecies paratuberculosis(MAP), elongation factor Tu (EF-Tu) and outer membrane porin C (ompC) fromEscherichia Coli(E. coli). Anti-microbial antibodies can cross-react to normal human tissues. The levels of antibodies against the microbial proteins are significantly elevated in the patients with CD and SS.ConclusionThe levels of antibodies against the microbial proteins are significantly elevated in CD and SS. The cross-reactivity of the anti-microbial antibodies to human tissue provides a new mechanism of pathogenesis of autoimmune diseases such as CD and SS.

Predictability of transcutaneous bilirubinometry in late preterm and term infants at risk for pathological hyperbilirubinemia

2020 ◽  
pp. 1-7
Author(s):  
E. Dianova ◽  
J. Fogel ◽  
R.P. Verma
Keyword(s):  
At Risk ◽  
Serum Bilirubin Level ◽  
Late Preterm ◽  
Term Infants ◽  
Term Neonates ◽  
Transcutaneous Bilirubin ◽  
Immune Mediated ◽  
Positive Direct ◽  
Neonatal Population ◽  
Transcutaneous Bilirubinometry

BACKGROUND: The aim was to assess the predictability of transcutaneous bilirubinometry in late preterm and term neonates at risk for pathological hyperbilirubinemia, and to identify the neonatal population in which transcutaneous bilirubin most accurately predicts serum bilirubin level (SB, mg/dl). METHODS: The correlations between transcutaneous bilirubin (TCB, mg/dl) and SB in different neonatal population subsets; and between ΔTSB (TCB-SB) and relevant neonatal variables and clinical groups were analyzed. RESULTS: TCB correlated with SB (r = 0.82, p <  0.05) in the cohort (n = 350) and in population subsets (r = 0.81–0.9, p <  0.001). Black infants with gestational age (GA) >35 weeks and chronological age (CA) >3 days recorded strongest correlation (r = 0.9, p <  0.001) followed by Blacks, and non-Black infants with CA >3 days and GA >35 weeks. ΔTSB was positive in Blacks, and in infants with CA <3 days, or with no phototherapy. ΔTSB was negative in non-Blacks, in infants with positive direct Coombs test (DC+) or those receiving phototherapy. Black race [beta (SE) = 1.3(0.33), p <  0.001] had positive, while CA [beta (SE) =−1.74 (0.36), p <  0.001], DC + status [beta (SE) =−0.72 (0.25), p = 0.004] and receipt of phototherapy [beta (SE) =−0.84 (0.21), p <  0.001] each had negative correlation with ΔTSB. ΔTSB for Blacks was >Whites, Hispanics and Asians. CONCLUSION: SB is best predicted by TCB in Black infants with CA over 3 days and GA over 35 weeks. Variability in SB estimation by TCB is race, CA and immune mediated hemolysis specific.

Autoimmune Comorbid Conditions in Multiple Sclerosis

US Neurology ◽  
2011 ◽  
Vol 07 (02) ◽  
pp. 132 ◽  
Author(s):  
Regina Berkovich ◽  
Dawood Subhani ◽  
Lawrence Steinman ◽  
◽  
◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Genetic Susceptibility ◽  
Interferon Beta ◽  
Comorbid Conditions ◽  
Factors Influencing ◽  
Immune Mediated ◽  
Autoimmune Conditions ◽  
Autoimmune Comorbidity

Autoimmune comorbidities occur frequently in multiple sclerosis (MS). They may arise as a consequence of a genetic susceptibility to autoimmunity. Certain pathological mechanisms are common to several autoimmune conditions. In the presence of comorbid autoimmune conditions, certain MS therapeutics may be preferable to others. Autoimmune comorbidity associated with MS could be a factor in predicting response to specific MS therapeutics. Treatment with interferon beta has been reported to precipitate immune-mediated abnormalities or to exacerbate existing autoimmune diseases. In comparison, there are fewer reported cases of treatment-associated comorbidities linked with autoimmune disease in patients taking glatiramer acetate. Knowledge of the factors influencing autoimmune comorbidities may provide insights into the complex pathogenesis of MS and help inform treatment choices.

Ciprofloxacin-induced immune-mediated thrombocytopenia: No cross-reactivity with gemifloxacin

2017 ◽  
Vol 43 (1) ◽  
pp. 134-136 ◽  
Author(s):  
D. W. Sim ◽  
J. E. Yu ◽  
J. Jeong ◽  
Y.-I. Koh
Keyword(s):  
Cross Reactivity ◽  
Immune Mediated

Inhibition of maturation and function of dendritic cells by intravenous immunoglobulin

Blood ◽  
2003 ◽  
Vol 101 (2) ◽  
pp. 758-765 ◽  
Author(s):  
Jagadeesh Bayry ◽  
Sébastien Lacroix-Desmazes ◽  
Cedric Carbonneil ◽  
Namita Misra ◽  
Vladimira Donkova ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Autoimmune Diseases ◽  
Intravenous Immunoglobulin ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cell Activity ◽  
Interleukin 12 ◽  
Immune Mediated ◽  
And Function

Normal immunoglobulin G for therapeutic use (intravenous immunoglobulin [IVIg]) is used in an increasing number of immune-mediated conditions, including acute and chronic/relapsing autoimmune diseases, transplantation, and systemic inflammatory disorders. Several mutually nonexclusive mechanisms of action account for the immunoregulatory effects of IVIg. Although IVIg inhibits T-cell proliferation and T-cell cytokine production, it is unclear whether these effects are directly dependent on the effects of IVIg on T cells or they are dependent through the inhibition of antigen-presenting cell activity. Here, we examined the effects of IVIg on differentiation, maturation, and function of dendritic cells (DCs). We show that IVIg inhibits the differentiation and maturation of DCs in vitro and abrogates the capacity of mature DC to secrete interleukin-12 (IL-12) on activation while enhancing IL-10 production. IVIg-induced down-regulation of costimulatory molecules associated with modulation of cytokine secretion resulted in the inhibition of autoreactive and alloreactive T-cell activation and proliferation. Modulation of DC maturation and function by IVIg is of potential relevance to its immunomodulatory effects in controlling specific immune responses in autoimmune diseases, transplantation, and other immune-mediated conditions.

scholarly journals Infectious Agents and Bone Marrow Failure: A Causal or a Casual Connection?

2021 ◽  
Vol 8 ◽  
Author(s):  
Valentina Giudice ◽  
Antonio M. Risitano ◽  
Carmine Selleri
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Failure ◽  
Indirect Evidence ◽  
Cell Receptor ◽  
Cross Reactivity ◽  
Autoimmune Response ◽  
Hematopoietic Stem ◽  
Immune Mediated ◽  
Viral Particles ◽  
Cellular Components

Acquired bone marrow failure (BMF) syndromes are considered immune-mediated disorders because hematological recovery after immunosuppressive therapies is the strongest indirect evidence of the involvement of immune cells in marrow failure development. Among pathophysiology hypotheses, immune derangement after chronic antigen exposure or cross-reactivity between viral particles and cellular components are the most accepted; however, epitopes against whom these lymphocytes are directed to remain unknown. In this study, we showed that BMF-associated immunodominant clones, namely the most represented T cells carrying an antigen-specific T-cell receptor (TCR) sequence in a random pool, were frequently associated with those described in various infectious diseases, such as cytomegalovirus (CMV) and Mycobacterium tuberculosis infection. We hypothesize that these pathogens might elicit an autoimmune response triggered by cross-reactivity between pathogen-related components and proteins or might be expanded as an unspecific response to a global immune dysregulation during BMF. However, those frequent intracellular pathogens might not only be passengers in marrow failure development, while playing a central role in starting the autoimmune response against hematopoietic stem cells.

Sign in / Sign up

Export Citation Format

Share Document