Microglia-specific localisation of a novel calcium binding protein, Iba1

Ito, Daisuke; Imai, Yoshinori; Ohsawa, Keiko; Nakajima, Kazuyuki; Fukuuchi, Yasuo; Kohsaka, Shinichi

doi:10.1016/s0169-328x(98)00040-0

Cited by 1,301 publications

(1,017 citation statements)

References 29 publications

Supporting

Mentioning

960

Contrasting

Unclassified

Order By: Relevance

“…The activated microglia markers IBA1 and CD68 exhibited a similar pattern of association with symptom duration, but CD68 association was stronger. IBA1 is a calcium-binding protein constitutively expressed in microglia and other macrophages and up-regulated in activated microglia, 53 whereas CD68 is a lysosomal marker specifically expressed by activated phagocytic cells. 54 Although the IBA1 protein levels are increased in the AD brain, we have previously shown that the number of IBA1 þ microglia detected by fluorescent immunohistochemistry does not substantially differ between AD and healthy control subjects.…”

Section: Discussionmentioning

confidence: 99%

Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease

Serrano-Pozo

Betensky

Frosch

et al. 2016

The American Journal of Pathology

View full text Add to dashboard Cite

Amyloid (senile) plaques, one of the two pathologic hallmarks of Alzheimer disease (AD), are associated with dystrophic neurites and glial responses, both astrocytic and microglial. Although plaque burden remains relatively stable through the clinical course of AD, whether these features of local plaque toxicity continue to worsen over the course of the disease is unclear. We performed an unbiased plaque-centered quantification of SMI312 þ dystrophic neurites, GFAP þ reactive astrocytes, and IBA1 þ and CD68 þ activated microglia in randomly selected dense-core (Thioflavin-S þ ) plaques from the temporal neocortex of 40 AD subjects with a symptom duration ranging from 4 to 20 years, and nine nondemented control subjects with dense-core plaques. Dystrophic neurites (Kendall t Z 0.34, P Z 0.001), reactive astrocytes (Kendall t Z 0.30, P Z 0.003), and CD68 þ (Kendall t Z 0.48, P < 0.0001), but not IBA1 microglia (Kendall t Z 0.045, P Z 0.655), exhibited a significant positive correlation with symptom duration. When excluding control subjects, only the positive association between CD68 þ microglia and symptom duration remained significant (Kendall t Z 0.39, P Z 0.0003). The presence of the APOEε4 allele did not affect these results. We conclude that plaques exert an increasing toxicity in the surrounding neuropil over the clinical course of AD, thereby potentially contributing to cognitive decline. (Am J Pathol 2016, 186: 375e384; http://dx

show abstract

Section: Discussionmentioning

confidence: 99%

Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease

Serrano-Pozo

Betensky

Frosch

et al. 2016

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Iba1 is a calcium-binding protein specifically expressed in microglia [65], which are activated in regions where cell death and inflammation occur (see, for example, [66]). Microglia were considered to be activated if they were present at high density and if they manifested an enlarged soma with relatively few cytoplasmic processes.…”

Section: Staining For Microgliamentioning

confidence: 99%

Reduction in 50-kHz call-numbers and suppression of tickling-associated positive affective behaviour after lesioning of the lateral hypothalamic parvafox nucleus in rats

Roccaro-Waldmeyer

Babalian

Müller

et al. 2016

Behavioural Brain Research

View full text Add to dashboard Cite

h i g h l i g h t s• Wistar rats were tickled before and after excitotoxic lesioning of the lateral hypothalamic parvafox nucleus.• Ultrasonic vocalisations (USVs) that were emitted during the tickling of rats and their tendency to approach and follow the experimenter's hand were analysed.• Lesioning was considered successful if the number of parvalbuminimmunoreactive (PV-ir) cells in the area of the parvafox nucleus was reduced beyond a threshold level.• Rats with bilaterally successful lesions manifested the most profound surgery-associated reduction in the number of 50-kHz USVs and in the tendency to approach and follow the experimenter's hand.• Positive correlations were found between each of the four investigated parameters. g r a p h i c a l a b s t r a c tThe parvafox nucleus is located ventrolaterally in the lateral hypothalamic area (LHA). Its core and shell are composed of neurons expressing the calcium-binding protein parvalbumin (PV) and the transcription factor Foxb1, respectively. Given the known functions of the LHA and that the parvafox nucleus receives afferents from the lateral orbitofrontal cortex and projects to the periaqueductal gray matter, a functional role of this entity in the expression of positive emotions has been postulated.The purpose of the present study was to ascertain whether the deletion of neurons in the parvafox nucleus influenced the tickling-induced 50-kHz calls, which are thought to reflect positive affective states, in rats. To this end, tickling of the animals (heterospecific play) was combined with intracerebral injections of the excitotoxin kainic acid into the parvafox nucleus.The most pronounced surgery-associated reduction in 50-kHz call-numbers was observed in the group of rats in which, on the basis of PV-immunoreactive-cell counts in the parvafox nucleus, bilateral lesions had been successfully produced. Two other parameters that were implemented to quantify positive affective behaviour, namely, an approach towards and a following of the hand of the tickling * Corresponding author at: Institute of Anatomy, University of Fribourg, Rte A. Gockel 1, CH-1700 Fribourg, Switzerland.E-mail address: marco.celio@unifr.ch (M.R. Celio). 1Published in which should be cited to refer to this work.http://doc.rero.ch experimenter, were likewise most markedly suppressed in the group of rats with bilaterally successful lesions. Furthermore, positive correlations were found between each of the investigated parameters. Our data afford evidence that the parvafox nucleus plays a role in the production of 50-kHz calls in rats, and, more generally, in the expression of positive emotions.

show abstract

“…Representative data from a mouse immunized 18 days previously with MOG are shown in Figure 3. Iba1, a marker of activated macrophages/microglia (Ito et al, 1998), was barely detectable in the brain stem/spinal cord of CFA-challenged Wt and LMP-2KO mice, but was much more readily detected in both mouse strains during EAE, indicative of widespread microglial activation during CNS demyelination ( Figure 3A). However, this activation was accompanied by only a slight increase in abundance: flow cytometric analyses of cells extracted from the same CNS samples ( Figure 3B) showed only a ~10% increase in the relative abundance of Mac-1 + cells during EAE, and this was true for both strains of mice.…”

Section: Histopathological Changes Mirror the Clinical Picturementioning

confidence: 99%

Myelin oligodendrocyte glycoprotein peptide-induced experimental allergic encephalomyelitis and T cell responses are unaffected by immunoproteasome deficiency

Frausto

Crocker

Eam

et al. 2007

Journal of Neuroimmunology

View full text Add to dashboard Cite

The inoculation of MOG peptides into C57BL/6 mice induces CD4 + and CD8 + T cells, and recent work has shown that adoptive transfer of the latter population, after extensive in vitro stimulation, can cause EAE in naïve recipient mice. Herein, we have evaluated the incidence and severity of EAE, and the induction of CD4 + and CD8 + T cells, following MOG peptide inoculation of wt mice and of LMP-2KO mice that lack an intact immunoproteasome, a cytoplasmic organelle that is induced by chronic inflammation and that may be important for the presentation of MHC class I epitopes to CD8 + T cells. We report that EAE, evaluated by both clinical and histological criteria, is similar in LMP-2KO mice and wildtype C57B/6 mice (wt) in response to immunization with MOG peptides MOG 35-55 and MOG [40][41][42][43][44][45][46][47][48][49][50][51][52][53][54] , suggesting that the immunoproteasome does not play a key role in the development of demyelinating disease. Furthermore, and consistent with previous reports, peptidespecific CD8 + T cells were barely detectable in the CNS of peptide-immunized mice, although peptide-specific CD4 + T cells were abundant. Therefore, we used a new technique to look for autoreactive CD8 + T cells in MOG peptide-immunized mice, and we report the identification of CD4 + and CD8 + T cells that, as late as 19 days after peptide injection, are actively producing IFNγ in vivo, in response to in vivo antigen contact.

show abstract

Microglia-specific localisation of a novel calcium binding protein, Iba1

Cited by 1,301 publications

References 29 publications

Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease

Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease

Reduction in 50-kHz call-numbers and suppression of tickling-associated positive affective behaviour after lesioning of the lateral hypothalamic parvafox nucleus in rats

Myelin oligodendrocyte glycoprotein peptide-induced experimental allergic encephalomyelitis and T cell responses are unaffected by immunoproteasome deficiency

Contact Info

Product

Resources

About