scholarly journals Regulation of B1 cell migration by signals through Toll-like receptors

2006 ◽  
Vol 203 (11) ◽  
pp. 2541-2550 ◽  
Author(s):  
Seon-ah Ha ◽  
Masayuki Tsuji ◽  
Keiichiro Suzuki ◽  
Bob Meek ◽  
Nobutaka Yasuda ◽  
...  
Keyword(s):  
Cell Migration ◽  
Immune Responses ◽  
High Velocity ◽  
Chemokine Receptors ◽  
Plasma Cells ◽  
Toll Like Receptors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
B1 Cells ◽  
Molecular Signals

Peritoneal B1 cells are known to generate large amounts of antibodies outside their residential site. These antibodies play an important role in the early defense against bacteria and viruses, before the establishment of adaptive immune responses. Although many stimuli, including antigen, lipopolysaccharide, or cytokines, have been shown to activate B1 cells and induce their differentiation into plasma cells, the molecular signals required for their egress from the peritoneal cavity are not understood. We demonstrate here that direct signals through Toll-like receptors (TLRs) induce specific, rapid, and transient down-regulation of integrins and CD9 on B1 cells, which is required for detachment from local matrix and a high velocity movement of cells in response to chemokines. Thus, we revealed an unexpected role for TLRs in governing the interplay between integrins, tetraspanins, and chemokine receptors required for B1 cell egress and, as such, in facilitating appropriate transition from innate to adaptive immune responses.

scholarly journals Toll-Like Receptors: Are They Taking a Toll on the Heart in Viral Myocarditis?

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1003
Author(s):  
Kasper Favere ◽  
Matthias Bosman ◽  
Karin Klingel ◽  
Stephane Heymans ◽  
Sophie Van Linthout ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Viral Myocarditis ◽  
Disease Process ◽  
Future Research ◽  
Toll Like Receptors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Evolutionarily Conserved

Myocarditis is an inflammatory disease of the heart with viral infections being the most common aetiology. Its complex biology remains poorly understood and its clinical management is one of the most challenging in the field of cardiology. Toll-like receptors (TLRs), a family of evolutionarily conserved pattern recognition receptors, are increasingly known to be implicated in the pathophysiology of viral myocarditis. Their central role in innate and adaptive immune responses, and in the inflammatory reaction that ensues, indeed makes them prime candidates to profoundly affect every stage of the disease process. This review describes the pathogenesis and pathophysiology of viral myocarditis and scrutinises the role of TLRs in every phase. We conclude with directions for future research in this field.

scholarly journals Role of Toll-Like Receptors in Neuroimmune Diseases: Therapeutic Targets and Problems

2021 ◽  
Vol 12 ◽  
Author(s):  
Haixia Li ◽  
Shan Liu ◽  
Jinming Han ◽  
Shengxian Li ◽  
Xiaoyan Gao ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Immune Responses ◽  
Inflammatory Responses ◽  
Inflammatory Factors ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Toll Like Receptors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Partial Activation

Toll-like receptors (TLRs) are a class of proteins playing a key role in innate and adaptive immune responses. TLRs are involved in the development and progression of neuroimmune diseases via initiating inflammatory responses. Thus, targeting TLRs signaling pathway may be considered as a potential therapy for neuroimmune diseases. However, the role of TLRs is elusive and complex in neuroimmune diseases. In addition to the inadequate immune response of TLRs inhibitors in the experiments, the recent studies also demonstrated that partial activation of TLRs is conducive to the production of anti-inflammatory factors and nervous system repair. Exploring the mechanism of TLRs in neuroimmune diseases and combining with developing the emerging drug may conquer neuroimmune diseases in the future. Herein, we provide an overview of the role of TLRs in several neuroimmune diseases, including multiple sclerosis, neuromyelitis optica spectrum disorder, Guillain-Barré syndrome and myasthenia gravis. Emerging difficulties and potential solutions in clinical application of TLRs inhibitors will also be discussed.

scholarly journals Chemokine Receptor Expression on Normal Blood CD56+NK-Cells Elucidates Cell Partners That Comigrate during the Innate and Adaptive Immune Responses and Identifies a Transitional NK-Cell Population

2015 ◽  
Vol 2015 ◽  
pp. 1-18 ◽  
Author(s):  
Margarida Lima ◽  
Magdalena Leander ◽  
Marlene Santos ◽  
Ana Helena Santos ◽  
Catarina Lau ◽  
...  
Keyword(s):  
Immune Responses ◽  
Nk Cells ◽  
Chemokine Receptors ◽  
Nk Cell ◽  
Cxcr4 Expression ◽  
Receptor Expression ◽  
Normal Blood ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Cd56 Expression

Studies of chemokine receptors (CKR) in natural killer- (NK-) cells have already been published, but only a few gave detailed information on its differential expression on blood NK-cell subsets. We report on the expression of the inflammatory and homeostatic CKR on normal bloodCD56+lowCD16+andCD56+high  CD16-/+lowNK-cells. ConventionalCD56+lowandCD56+highNK-cells present in the normal PB do express CKR for inflammatory cytokines, although with different patternsCD56+lowNK-cells are mainly CXCR1/CXCR2+and CXCR3/CCR5−/+, whereas mostlyCD56+highNK-cells are CXCR1/CXCR2−and CXCR3/CCR5+. Both NK-cell subsets have variable CXCR4 expression and are CCR4−and CCR6−. The CKR repertoire of theCD56+lowNK-cells approaches to that of neutrophils, whereas the CKR repertoire of theCD56+highNK-cells mimics that of Th1+T cells, suggesting that these cells are prepared to migrate into inflamed tissues at different phases of the immune response. In addition, we describe a subpopulation of NK-cells with intermediate levels of CD56 expression, which we namedCD56+intNK-cells. These NK-cells are CXCR3/CCR5+, they have intermediate levels of expression of CD16, CD62L, CD94, and CD122, and they are CD57−and CD158a−. In view of their phenotypic features, we hypothesize that they correspond to a transitional stage, between the well-knownCD56+highandCD56+lowNK-cells populations.

Toll-like receptors control activation of adaptive immune responses

10.1038/ni712 ◽  
2001 ◽  
Vol 2 (10) ◽  
pp. 947-950 ◽  
Author(s):  
Markus Schnare ◽  
Gregory M. Barton ◽  
Agnieszka Czopik Holt ◽  
Kiyoshi Takeda ◽  
Shizuo Akira ◽  
...  
Keyword(s):  
Immune Responses ◽  
Toll Like Receptors ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Control Activation

scholarly journals The Role of Toll-Like Receptors in Retroviral Infection

2020 ◽  
Vol 8 (11) ◽  
pp. 1787
Author(s):  
Edward P. Browne
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune Responses ◽  
Toll Like Receptors ◽  
Adaptive Immune Responses ◽  
Retroviral Infection ◽  
Functional Roles ◽  
Adaptive Immune ◽  
Immunodeficiency Virus ◽  
Growing Body

Toll-like receptors (TLRs) are key pathogen sensing receptors that respond to diverse microbial ligands, and trigger both innate and adaptive immune responses to infection. Since their discovery, a growing body of evidence has pointed to an important role for TLRs in retroviral infection and pathogenesis. These data suggest that multiple TLRs contribute to the anti-retroviral response, and that TLR engagement by retroviruses can have complex and divergent outcomes for infection. Despite this progress, numerous questions remain about the role of TLRs in retroviral infection. In this review, I summarize existing evidence for TLR-retrovirus interactions and the functional roles these receptors play in immunity and pathogenesis, with particular focus on human immunodeficiency virus (HIV).

Sign in / Sign up

Export Citation Format

Share Document