Attenuated demyelination in the absence of the macrophage-restricted adhesion molecule sialoadhesin (Siglec-1) in mice heterozygously deficient in P0

Kobsar, Igor; Oetke, Cornelia; Kroner, Antje; Wessig, Carsten; Crocker, Paul R.; Martini, Rudolf

doi:10.1016/j.mcn.2005.12.007

Cited by 37 publications

(20 citation statements)

References 27 publications

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“…Since it lacks tyrosine binding signaling motifs within its cytoplasmic domain and this domain is poorly conserved, it is likely that its primary function is more to serve as a binding partner for appropriate ligands and involved in cell adhesion and functions such as serving as a phagocyte receptor [42]. It has also been implicated in influencing T cell function and activation [43]. Increased expression of Siglec-1 following SIV infection in RM but not SM suggests that the above noted functions are likely to be perturbed following SIV infection of RM.…”

Section: Discussionmentioning

confidence: 99%

Differences in the constitutive and SIV infection induced expression of Siglecs by hematopoietic cells from non-human primates

Jaroenpool

Rogers

Pattanapanyasat

et al. 2007

Cellular Immunology

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The expression of the Siglec family of molecules by hematopoietic cells from uninfected and SIV infected disease susceptible rhesus macaques (RM) and SIV infected disease resistant sooty mangabeys (SM) and for comparison humans was carried out. The predominant cell lineage in all 3 species expressing Siglec's was monocytes. The major finding by both a cross sectional and a prospective SIV infection study showed that whereas monocytes from RM show marked increase in each Siglec constitutively expressed, monocytes from SM showed marked decreases in Siglec-1 expression. While monocytes from all 3 species constitutively expressed Siglec-3, human monocytes in addition expressed Siglec-5 and 9 and to a lower density 7, monocytes from RM expressed Siglec-7 and those from SM expressed Siglec-1. Monocytes from all 3 species however expressed mRNA for Siglec's-1, 5, 7 and 9. The reasons for the failure to detect these molecules at the protein level and the mechanisms for such distinct effects of SIV infection on Siglec expression are discussed.

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Section: Discussionmentioning

confidence: 99%

Differences in the constitutive and SIV infection induced expression of Siglecs by hematopoietic cells from non-human primates

Jaroenpool

Rogers

Pattanapanyasat

et al. 2007

Cellular Immunology

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“…Currently, it is unclear to what extent activation of the immune system contributes to the peripheral neuropathy observed in our tamoxifen-treated mice. Analysis of several other myelin mutants including Mpz, Pmp22, and Cx32 mice has shown, however, that macrophage activation strongly contributes to the observed peripheral nerve damage, but also paves the way for repair (Carenini et al, 2001;Kobsar et al, 2002Kobsar et al, , 2005Kobsar et al, , 2006; reviewed in Martini et al, 2008). Therefore, it will be interesting in future studies to dissect the contribution of neuroinflammatory processes to the peripheral neuropathy elicited by Sox10 deletion in the adult.…”

Section: Sox2mentioning

confidence: 99%

Sox10 is required for Schwann‐cell homeostasis and myelin maintenance in the adult peripheral nerve

Bremer

Fröb

Kichko

et al. 2011

Glia

120

122

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The transcription factor Sox10 functions during multiple consecutive stages of Schwann-cell development in the peripheral nervous system (PNS). Although Sox10 continues to be expressed in mature Schwann cells of the adult peripheral nerve, it is currently unclear whether it is still functional. Here, we used a genetic strategy to selectively delete Sox10 in glia of adult mice in a tamoxifen-dependent manner. The tamoxifen-treated mice developed a severe peripheral neuropathy that was associated with dramatic alterations in peripheral nerve structure and function. Demyelination and axonal degeneration were as much evident as signs of neuroinflammation. Compound action potentials exhibited pathophysiological alterations. Sox10-deleted Schwann cells persisted in the peripheral nerve, but did not exhibit a mature, myelinating phenotype arguing that Sox10 is rather required for differentiation and maintenance of the differentiated state than for survival. Our report is the first evidence that Sox10 is still essentially required for Schwann-cell function in the adult PNS and establishes a useful model in which to study human peripheral neuropathies.

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“…In addition to their presence in peripheral tissues, CD169 + macrophages are found in the marginal zone of secondary lymphoid organs, where they can promote immune tolerance to soluble antigens and antigens expressed by dead cells (10,11). Paradoxically, CD169 + tissue-resident macrophages, or subsets thereof, can also promote pathogenic central nervous system autoimmunity (12)(13)(14) and antitumor immunity (15). Although CD169 + macrophages are present in many tissues, including skin (6), heart (16), and pancreas (17) in mice and lung, colon, and liver in humans (18), their role in shaping adaptive alloimmune responses and the potential for subpopulations remains enigmatic.…”

Section: Introductionmentioning

confidence: 99%

Fragile TIM-4–expressing tissue resident macrophages are migratory and immunoregulatory

Thornley¹,

Fang²,

Balasubramanian³

et al. 2014

J. Clin. Invest.

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Attenuated demyelination in the absence of the macrophage-restricted adhesion molecule sialoadhesin (Siglec-1) in mice heterozygously deficient in P0

Cited by 37 publications

References 27 publications

Differences in the constitutive and SIV infection induced expression of Siglecs by hematopoietic cells from non-human primates

Differences in the constitutive and SIV infection induced expression of Siglecs by hematopoietic cells from non-human primates

Sox10 is required for Schwann‐cell homeostasis and myelin maintenance in the adult peripheral nerve

Fragile TIM-4–expressing tissue resident macrophages are migratory and immunoregulatory

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