Review Article
Adaptive Immunity and Antigen-Specific Activation in Obesity-Associated Insulin Resistance
Table 1
Evidence for antigen-specific mechanisms in obesity-associated IR.
| | Source |
| Direct evidence of antigen-specific pathology | | MHC-II presentation of antigen is necessary for metabolic defects | [61, 62, 98] | VAT-specific TCR repertoire restriction in obese IR mice | [22, 34, 44] | Expansion of effector memory T cells is MHC-II dependent | [98] | Regulation of glucose intolerance is not achieved by transfer of CD4+ OT-2 T cells | [22] | Transfer of disease by antibody is dependent on metabolic status of source and recipient mice | [40] | Insulin resistant and insulin sensitive individuals have distinct IgG autoantibody signatures | [40] | Indirect evidence of antigen-specific activation | | Enrichment of antibody within crown-like structures | [40] | Enrichment of T cells within crown-like structures | [10] | Expansion of effector memory T cells in obesity is specific to the adipose tissue | [43, 98] | Antibody class switching is increased in obesity | [40] | Contradictory evidence | | No HLA linkage in type 2 diabetes | [99] | No T cell or B cell specific genes linked to type 2 diabetes | [100, 101] | Costimulation is beneficial for glucose metabolism or lack of costimulation worsens glucose metabolism | [102–104] |
|
|