CD4⁺T Cells Promote Antibody Production but Not Sustained Affinity Maturation during Borrelia burgdorferi Infection

sIgM–FcμR Interactions Regulate Early B Cell Activation and Plasma Cell Development after Influenza Virus Infection

“…Antibody-binding was revealed with goat anti-mouse IgM and IgG, IgG1, IgG2a, IgG2c, IgG3 biotin (Southern Biotech) and with SA-HPO (Vector) incubated each for 1 hour. The avidity index for A/PR8 specific IgG and IgG1 binding was measured by conducting virus-specific ELISAs in the presence or absence of a 5M urea wash following antibody-binding as described previously (35). …”

A small intergenic region of lp17 is required for evasion of adaptive immunity and induction of pathology by the Lyme disease spirochete

“…Although the previous results characterising dbpA/B-deficient B. burgdorferi do not perfectly mirror the dissemination kinetics reported in this study, they provide precedence for the early colonisation defect observed here in an adaptive immune-dependent manner, as well as the finding that Δ1-7 gradually increased in bacterial burden over time to wild-type levels in the joints. During infection with B. burgdorferi, the effective adaptive immune mechanisms capable of modulating bacterial burden and disease severity are primarily antibody mediated and are characterised by a robust early T cellindependent antibody response in addition to T cell-dependent antibodies (Barthold & Bockenstedt, 1993;Barthold, deSouza, & Feng, 1996;Barthold, Feng, Bockenstedt, Fikrig, & Feen, 1997;Elsner et al, 2015;Hastey et al, 2012;McKisic & Barthold, 2000;Tunev et al, 2011). Susceptibility of B. burgdorferi to antibodies varies temporally throughout infection, potentially due to the adaptation state of the bacteria in the host.…”

“…Lyme disease is the most prevalent vector‐borne infectious disease in North America, and infection with the causative bacterial spirochete, Borrelia burgdorferi , can result in debilitating clinical manifestations in humans including arthritis and carditis (Bratton, Whiteside, Hovan, Engle, & Edwards, ; Steere et al, ; Steere & Glickstein, ; Steere, Schoen, & Taylor, ). B. burgdorferi is capable of persisting in an infected mammalian host in the presence of adaptive immune responses through both alterations in the antigenic profile of the bacterium (Liang et al, , Liang, Nelson, & Fikrig, , Liang, Nelson, & Fikrig, , Samuels, , Singh & Girschick, ) and by modulation of the host's antibody responses (Elsner, Hastey, & Baumgarth, ; Hastey, Elsner, Barthold, & Baumgarth, ; Tunev et al, ). The presence of live spirochetes in heart and synovial joints is associated with subacute inflammation in C3H mice that exhibits parallels with inflammatory disease seen in humans.…”

Borrelia-associated Fasciitis: Two Cases

“…It had been suggested that Borrelia spp. infection drives the humoral response away from protective, high-affinity, and long-lived antibody responses and toward the rapid induction of strongly induced, short-lived antibodies of limited efficacy, explaining the presence of IgM and the absence of IgG in our case (15).…”