Autoimmunity in Primary Immunodeficiencies (PID)

Padron, Grace T.; Hernandez-Trujillo, Vivian

doi:10.1007/s12016-022-08942-0

Cited by 8 publications

(9 citation statements)

References 207 publications

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“…Peripheral tolerance is induced by CD4Treg, CD8Treg, T FR , and Breg cells that regulate GC reaction by multiple mechanisms, including anergy, apoptosis, and suppression of effector functions of self-reacting T and B cells [reviewed in [ 54 ]]. Since patients with PAD, especially CVID, develop autoimmunity and their alterations have been reported in CVID [ 55 ], we studied their relative proportions following two doses of the SARS-CoV-2 vaccine. The data are shown in Figure 10 .…”

Section: Resultsmentioning

confidence: 99%

Adaptive Cellular Responses following SARS-CoV-2 Vaccination in Primary Antibody Deficiency Patients

Gupta,

Su,

Agrawal

et al. 2024

Pathogens

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Since the start of the COVID-19 pandemic, in a short span of 3 years, vaccination against SARS-CoV-2 has resulted in the end of the pandemic. Patients with inborn errors of immunity (IEI) are at an increased risk for SARS-CoV-2 infection; however, serious illnesses and mortality, especially in primary antibody deficiencies (PADs), have been lower than expected and lower than other high-risk groups. This suggests that PAD patients may mount a reasonable effective response to the SARS-CoV-2 vaccine. Several studies have been published regarding antibody responses, with contradictory reports. The current study is, perhaps, the most comprehensive study of phenotypically defined various lymphocyte populations in PAD patients following the SARS-CoV-2 vaccine. In this study, we examined, following two vaccinations and, in a few cases, prior to and following the 1st and 2nd vaccinations, subsets of CD4 and CD8 T cells (Naïve, TCM, TEM, TEMRA), T follicular helper cells (TFH1, TFH2, TFH17, TFH1/17), B cells (naïve, transitional, marginal zone, germinal center, IgM memory, switched memory, plasmablasts, CD21low), regulatory lymphocytes (CD4Treg, CD8Treg, TFR, Breg), and SARS-CoV-2-specific activation of CD4 T cells and CD8 T cells (CD69, CD137), SARS-CoV-2 tetramer-positive CD8 T cells, and CD8 CTL. Our data show significant alterations in various B cell subsets including Breg, whereas only a few subsets of various T cells revealed alterations. These data suggest that large proportions of PAD patients may mount significant responses to the vaccine.

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Section: Resultsmentioning

confidence: 99%

Adaptive Cellular Responses following SARS-CoV-2 Vaccination in Primary Antibody Deficiency Patients

Gupta,

Su,

Agrawal

et al. 2024

Pathogens

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“…It may also facilitate the reactivation of latent viruses. In addition, T4 deficiency is known to provoke immune activation and autoimmunity ( 30 ). Immune activation is also known to provoke endothelial cell activation and coagulation ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID

Cezar,

Kundura,

André

et al. 2024

Front. Immunol.

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BackgroundAs about 10% of patients with COVID-19 present sequelae, it is important to better understand the physiopathology of so-called long COVID.MethodTo this aim, we recruited 29 patients hospitalized for SARS-CoV-2 infection and, by Luminex®, quantified 19 soluble factors in their plasma and in the supernatant of their peripheral blood mononuclear cells, including inflammatory and anti-inflammatory cytokines and chemokines, Th1/Th2/Th17 cytokines, and endothelium activation markers. We also measured their T4, T8 and NK differentiation, activation, exhaustion and senescence, T cell apoptosis, and monocyte subpopulations by flow cytometry. We compared these markers between participants who developed long COVID or not one year later.ResultsNone of these markers was predictive for sequelae, except programmed T4 cell death. T4 lymphocytes from participants who later presented long COVID were more apoptotic in culture than those of sequelae-free participants at Month 12 (36.9 ± 14.7 vs. 24.2 ± 9.0%, p = 0.016).ConclusionsOur observation raises the hypothesis that T4 cell death during the acute phase of SARS-CoV-2 infection might pave the way for long COVID. Mechanistically, T4 lymphopenia might favor phenomena that could cause sequelae, including SARS-CoV-2 persistence, reactivation of other viruses, autoimmunity and immune dysregulation. In this scenario, inhibiting T cell apoptosis, for instance, by caspase inhibitors, could prevent long COVID.

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“…Overall, our results suggest that the albino phenotype encompasses far more than a pigmentation defect; rather, it represents a systematic problem associated with the immune system. This could explain the concomitant physiological defects, such as malformation, delayed growth, and mortality at early development ( 33 ), as immune activity can be linked to growth and development performance through both resource allocation ( 34 ) and crosstalk between regulation pathways ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

Albinism in the largest extant amphibian: A metabolic, endocrine, or immune problem?

Zhu

Jiang

2022

Front. Endocrinol.

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BackgroundPigment regression is an intriguing phenomenon that can be caused by disorders in melanin metabolism or endocrine regulation, or by autoimmune disorders. Albino animals serve as excellent models for the study of the genetic determination of morphology, particularly the evolution of and molecular mechanisms underlying chromatophore-related diseases in animals and humans.Material and MethodsThe artificial culture of Andrias davidianus, the largest extant amphibian, is flourishing in China due to the great ecological and economic value of this animal. Approximately 0.1% of individuals express an albino phenotype accompanied by delayed somatic growth and mortality at early developmental stages. In this study, brain and skin transcriptomics were conducted to study the underlying molecular basis of the phenotype.ResultsThe results indicated decreased transcription of genes of melanin synthesis. Interestingly, MHC I isotypes and immune-related pathways accounted for the primary transcriptional differences between groups, suggesting that the albino phenotype represents a systematic immune problem to a far greater extent than a pigmentation defect. Albino individuals exhibited shifted transcription of MHC I isotypes, and the albino-specific isotype was characterized by increased charges and decreased space in the antigen- binding pocket, implying a drastic change in antigen specificity and a potential risk of autoimmune disorders.ConclusionThese results suggest an association between the albino phenotype and MHC I variants in A. davidianus, which could serve as a convenient model for vitiligo or other autoimmune diseases.

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Autoimmunity in Primary Immunodeficiencies (PID)

Cited by 8 publications

References 207 publications

Adaptive Cellular Responses following SARS-CoV-2 Vaccination in Primary Antibody Deficiency Patients

Adaptive Cellular Responses following SARS-CoV-2 Vaccination in Primary Antibody Deficiency Patients

T4 apoptosis in the acute phase of SARS-CoV-2 infection predicts long COVID

Albinism in the largest extant amphibian: A metabolic, endocrine, or immune problem?

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