burgdorferi. quantity of recombinant Borrelia-antigens. Finally, neither the quality nor the magnitude of the B cell responses was modified in mice missing the Toll-like receptor adaptor molecule MyD88. With each other, these findings suggest a novel evasion strategy forB. burgdorferi: subversion of the quality of a strongly induced, potentially protecting borrelia-specific antibody response viaB. burdorferi’s build up in lymph nodes. == Author Summary == Acute Lyme Disease is one of the most important growing diseases in the US. People with acute Lyme disease often develop swollen lymph nodes, or lymphadenopathy, but we do not know why this happens or what effect it has on the course of the disease. We show here that when mice are infected with liveBorrelia burgdorferispirochetes (the bacteria that cause Lyme disease), live spirochetes collect in the lymph nodes. These lymph nodes then swell up and start producing large numbers of antibody-producing cells. Although many of these antibodies can identify the bacteria, they apparently lack the quality to obvious the infection. We hypothesize that by moving into the lymph node, usually a site in which strong immune responses are induced, Borrelia evades the immune response: it goes to the lymph nodes and methods the immune system into making a very strong but inadequate response. == Intro == Lyme borreliosis, caused byBorrelia burgdorferitransmitted byIxodes spp.ticks, is the most common arthropod-borne illness in the US and Europe, and is increasing in prevalence and expanding in geographic distribution in the US[1],[2]. Clinical manifestations are highly varied, including involvement of the cutaneous, cardiovascular, musculoskeletal, and nervous systems[3][5]. A frequent, but mainly under-studied manifestation is usually massive and systemic lymph node enlargement (lymphadenopathy), observed particularly in the regional lymph node near the site of illness in humans, and in experimentally-infected dogs[4],[6]. The lymph node enlargement that occurs in both humans and dogs is usually characterized by increased cellularity and the build up of large pleomorphic IgM- and IgG-positive plasma cells[6][8]. Despite these unusual characteristics, the lymphadenopathy of Lyme borreliosis has not been well investigated. Severalin vitrostudies have shown that culture-grownB. burgdorferican act as mitogens when co-cultured with human being or murine naive B cells[9][16]. Consequently, the unusual lymphadenopathy of Lyme KLHL11 antibody borreliosis might be a manifestation of non-specific B cell activation. Massive lymph node enlargement has also been seen in wildtype but not TLR4 gene-targeted mice during illness withSalmonella typhimurium[17]and others have shown a role for TLR-independent, TNF-independent[18]or TNF-dependent[19]involvement of mast cells in non-specific induction of lymph node enlargement. Thus, innate ADL5747 immune activation might account for the lymphadenopathy observed during illness withB. burgdorferi. On the other hand, there is ample evidence for the induction of specific immune responses followingB. burgdorferiinfection. Both following experimental and natural infections,B. burgdorferi-specific IgM and IgG antibodies ADL5747 are induced in the serum of infected humans[5],[20][24], dogs[25], and mice[26], among additional host species. Importantly, passive transfer of immune-serum from chronically infected wildtype or T cell-deficient mice, ADL5747 from naturally infected dogs, and from human being individuals with chronic Lyme disease can protect mice from challenging illness withB. burgdorferi[26][29], demonstrating that specific and protecting antibodies are induced during the course of illness. However, once illness is made, the immune response is incapable of clearing illness[26],[30]. Therefore, understanding the sponsor immune response is critical to understanding and treating Lyme borreliosis. The present.