Maternal provisions in type 1 diabetes: Evidence for both protective & pathogenic potential

Front Immunol. 2023 Mar 22:14:1146082. doi: 10.3389/fimmu.2023.1146082. eCollection 2023.

Abstract

Maternal influences on the immune health and development of an infant begin in utero and continue well into the postnatal period, shaping and educating the child's maturing immune system. Two maternal provisions include early microbial colonizers to initiate microbiota establishment and the transfer of antibodies from mother to baby. Maternal antibodies are a result of a lifetime of antigenic experience, reflecting the infection history, health and environmental exposure of the mother. These same factors are strong influencers of the microbiota, inexorably linking the two. Together, these provisions help to educate the developing neonatal immune system and shape lymphocyte repertoires, establishing a role for external environmental influences even before birth. In the context of autoimmunity, the transfer of maternal autoantibodies has the potential to be harmful for the child, sometimes targeting tissues and cells with devastating consequences. Curiously, this does not seem to apply to maternal autoantibody transfer in type 1 diabetes (T1D). Moreover, despite the rising prevalence of the disease, little research has been conducted on the effects of maternal dysbiosis or antibody transfer from an affected mother to her offspring and thus their relevance to disease development in the offspring remains unclear. This review seeks to provide a thorough evaluation of the role of maternal microorganisms and antibodies within the context of T1D, exploring both their pathogenic and protective potential. Although a definitive understanding of their significance in infant T1D development remains elusive at present, we endeavor to present what has been learned with the goal of spurring further interest in this important and intriguing question.

Keywords: autoantibody; autoimmunity; dysbiosis; immunoglobulin; microbiome; tolerance.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Autoantibodies
  • Autoimmunity
  • Child
  • Diabetes Mellitus, Type 1*
  • Female
  • Humans
  • Immune System
  • Infant
  • Infant, Newborn
  • Mothers

Substances

  • Autoantibodies

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