Downregulation of class II molecules on epidermal Langerhans cells in Lyme borreliosis

Silberer, M.; Koszik, Frieder; Stingl, Georg; Aberer, Elisabeth

doi:10.1046/j.1365-2133.2000.03776.x

Cited by 28 publications

(19 citation statements)

References 31 publications

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“…Langerhans cells are present in erythema migrans, and their number is increased in acrodermatitis chronica atrophicans, the late skin manifestation of LB, but the MHC II expression of these cells is decreased in both lesions (38). B. burgdorferi sensu stricto can also be isolated from both of these skin lesions (39).…”

Section: Discussionmentioning

confidence: 94%

TLR2 Utilization ofBorreliaDoes Not Induce p38- and IFN-β Autocrine Loop-Dependent Expression of CD38, Resulting in Poor Migration and Weak IL-12 Secretion of Dendritic Cells

Hartiala

Hytönen²,

Yrjänäinen³

et al. 2010

The Journal of Immunology

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Lyme borreliosis is a tick-borne bacterial infection that in many cases is limited to the skin. However, in some patients the bacterium evades the immune response and disseminates into various organs. Dendritic cells (DCs) are among the first cells to meet invading pathogens in the skin. We have previously shown that CD38, an ectoenzyme involved in the migration of DCs and generally upregulated by microbial stimuli, is not upregulated in Borrelia garinii-stimulated DCs. In this paper, we characterize the cellular events that lead to the absence of CD38 on the DC surface after B. garinii stimulation and investigate the consequences of absent CD38 expression for the migration of DCs in vitro and in vivo. The data show that 1) effective signaling via p38 MAPK (and STAT1 and NF-κB) is needed for CD38 expression and 2) TLR2 stimulation, as opposed to TLR4 stimulation, does not induce IFN-β autocrine loop-dependent expression of CD38 and secretion of IL-12. Further, we show that 3) B. garinii-stimulated DCs do not migrate effectively toward CCL19 and CCL21 and 4) after B. garinii infection of mice, the number of DCs migrating from the infection site to draining lymph nodes is only half that induced by Escherichia coli infection. Our results provide evidence for the first time that different TLR use results in different CD38 expression, which correlates with the migratory potential of DCs.

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Section: Discussionmentioning

confidence: 94%

TLR2 Utilization ofBorreliaDoes Not Induce p38- and IFN-β Autocrine Loop-Dependent Expression of CD38, Resulting in Poor Migration and Weak IL-12 Secretion of Dendritic Cells

Hartiala

Hytönen²,

Yrjänäinen³

et al. 2010

The Journal of Immunology

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“…The inflammatory infiltrate in both the early and late skin manifestations of Lyme borreliosis is mainly composed of CD68 þ macrophages and CD45RO þ memory T cells, with a predominance of CD4 þ helper T cells (Silberer et al, 2000). Epidemiological data from many countries show that LD has increased significantly in incidence since the 1980s (Jaenson, 1991;Strle, 1999).…”

Section: Discussionmentioning

confidence: 99%

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

et al. 2006

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Mycosis fungoides (MF) is the most frequently found cutaneous T-cell lymphoma with an unknown aetiology. Several aetiopathogenetic mechanisms have been postulated, including persistent viral or bacterial infections. We looked for evidence of Borrelia burgdorferi (Bb), the aetiologic agent of Lyme disease (LD), in a case study of MF patients from Northeastern Italy, an area with endemic LD. Polymerase chain reaction for the flagellin gene of Bb was used to study formalin-fixed paraffin-embedded lesional skin biopsies from 83 patients with MF and 83 sex-and age-matched healthy controls with homolocalised cutaneous nevi. Borrelia burgdorferi-specific sequence was detected in 15 out of 83 skin samples of patients with MF (18.1%), but in none out of 83 matched healthy controls (Po0.0001). The Bb positivity rates detected in this study support a possible role for Bb in the aetiopathogenesis of MF in a population endemic for LD.

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“…The inoculation of the bacteria by the tick bite results after a few days in a characteristic rash, erythema migrans, which may be accompanied by systemic symptoms, including malaise, fatigue, fever, headache, neck stiffness, arthralgias, or myalgias (30,51,58). Adhesion, colonization, and proliferation within the skin and other host organs and tissues by B. burgdorferi necessitates interaction between the spirochete and cells of the connective tissue, including macrophages, dendritic cells, fibroblasts (24,48), and the associated extracellular matrix (ECM) (24).B. burgdorferi expresses cell surface proteins that interact specifically with different components of the ECM of the host organism and of mammalian cells in culture (8,23,26,30).…”

mentioning

confidence: 99%

Borrelia burgdorferi Binds to, Invades, and Colonizes Native Type I Collagen Lattices

Zambrano¹,

Beklemisheva²,

Bryksin³

et al. 2004

Infect Immun

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Borrelia burgdorferi binds strongly to the extracellular matrix and cells of the connective tissue, a binding apparently mediated by specific proteins and proteoglycans. We investigated the interactions between B. burgdorferi cells and intact type I collagen using hydrated lattices that reproduce features of in vivo collagen matrices. B. burgdorferi cells of several strains adhered avidly to these acellular matrices by a mechanism that was not mediated by decorin or other proteoglycans. Moreover, following adhesion to these matrices, B. burgdorferi grew and formed microcolonies. The collagen used in these studies was confirmed to lack decorin by immunoblot analysis; B. burgdorferi cells lacking the decorin adhesin bound readily to intact collagen matrices. B. burgdorferi also bound to collagen lattices that incorporated enzymes that degraded glycosaminoglycan chains in any residual proteoglycans. Binding of the bacteria to intact collagen was nonetheless specific, as bacteria did not bind agar and showed only minimal binding to bovine serum albumin, gelatin, pepsinized type I collagen, and intact collagen that had been misassembled under nonphysiological pH and ionic-strength conditions. Proteinase K treatment of B. burgdorferi cells decreased the binding, as did a lack of flagella, suggesting that surface-exposed proteins and motility may be involved in the ability of B. burgdorferi to interact with intact collagen matrices. The high efficiency of binding of B. burgdorferi strains to intact collagen matrices permits replacement of the commonly used isotopic binding assay with visual fluorescent microscopic assays and will facilitate future studies of these interactions.Borrelia burgdorferi, the etiologic agent of Lyme disease, is transmitted to animals and humans mainly by nymphae of the tick Ixodes scapularis, which during a blood meal deposit a small number of microorganisms into the skin (8,43,51). The inoculation of the bacteria by the tick bite results after a few days in a characteristic rash, erythema migrans, which may be accompanied by systemic symptoms, including malaise, fatigue, fever, headache, neck stiffness, arthralgias, or myalgias (30,51,58). Adhesion, colonization, and proliferation within the skin and other host organs and tissues by B. burgdorferi necessitates interaction between the spirochete and cells of the connective tissue, including macrophages, dendritic cells, fibroblasts (24,48), and the associated extracellular matrix (ECM) (24).B. burgdorferi expresses cell surface proteins that interact specifically with different components of the ECM of the host organism and of mammalian cells in culture (8,23,26,30). These B. burgdorferi surface proteins include the fibronectin receptor encoded by BBK32 (42); proteins that bind directly to glycosaminoglycans (GAGs), such as Bgp (39-41); and membrane lipoproteins, such as DbpA and DbpB, which bind to decorin (4,16,(20)(21)(22). The B. burgdorferi outer membrane protein p66 binds to the beta3 integrin chain of host ECM receptors (9-12). The var...

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Downregulation of class II molecules on epidermal Langerhans cells in Lyme borreliosis

Cited by 28 publications

References 31 publications

TLR2 Utilization ofBorreliaDoes Not Induce p38- and IFN-β Autocrine Loop-Dependent Expression of CD38, Resulting in Poor Migration and Weak IL-12 Secretion of Dendritic Cells

TLR2 Utilization ofBorreliaDoes Not Induce p38- and IFN-β Autocrine Loop-Dependent Expression of CD38, Resulting in Poor Migration and Weak IL-12 Secretion of Dendritic Cells

Mycosis fungoides: is it a Borrelia burgdorferi-associated disease?

Borrelia burgdorferi Binds to, Invades, and Colonizes Native Type I Collagen Lattices

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