Alphab-crystallin is a target for adaptive immune responses and a trigger of innate responses in preactive multiple sclerosis lesions.

We present the first comparative analysis of serum immunoglobulin G reactivity profiles against the full spectrum of human myelin-associated proteins in multiple sclerosis patients and healthy control subjects. In both groups, serum antibodies display a consistent and prominent reaction to alphaB-crystallin (CRYAB) versus other myelin proteins. As an apparently major target for the adaptive immune system in humans, CRYAB selectively accumulates in oligodendrocytes, but not in astrocytes, or axons in so-called preactive multiple sclerosis lesions.

Enhanced expression of lmb gene encoding laminin-binding protein in Streptococcus agalactiae strains harboring IS1548 in scpB-lmb intergenic region.

Group B streptococcus (GBS) is the main cause of neonatal sepsis and meningitis. Bacterial surface proteins play a major role in GBS binding to and invasion of different host surfaces. The scpB and lmb genes, coding for fibronectin-binding and laminin-binding surface proteins, are present in almost all human GBS isolates.

The microtubule regulator stathmin is an endogenous protein agonist for TLR3.

TLR3 recognizes dsRNAs and is considered of key importance to antiviral host-defense responses. TLR3 also triggers neuroprotective responses in astrocytes and controls the growth of axons and neuronal progenitor cells, suggesting additional roles for TLR3-mediated signaling in the CNS. This prompted us to search for alternative, CNS-borne protein agonists for TLR3.

Trophic factors and stem cells for promoting recovery in stroke.

Background: Stem cell therapy for stroke is in its initial stages as an option to restore lost neurological functions after stroke.

Objective: To provide a comprehensive review of studies involving stem cells in stroke treatment and to highlight new evidence from the ongoing clinical trials.

Methodology: We performed a systematic study of various published journals in online medical libraries using Pubmed, Sciencedirect, and hajournal.

Zinc, copper and antioxidant enzyme activities in healthy elderly Tunisian subjects.

Trace elements like zinc and copper play an important role in maintaining metabolic homeostasis in elderly subjects and is therefore expected to have a crucial effect on antioxidant mechanism. The objective of the present study was to investigate age-related variations of zinc, copper and antioxidant enzyme activities (superoxide dismutase: SOD, glutathione peroxidase: GPx and catalase: CAT) taking into account gender differences in a Tunisian elderly population. A group of 100 healthy elderly subjects (55-85 years old) were then separated in three sub-groups according to age intervals.

Unusual case of thiamine responsive megaloblastic anemia.

Background: Thiamine-responsive megaloblastic anemia syndrome is a rare autosomal recessive disorder defined by the occurrence of megaloblastic anemia, diabetes mellitus, and neurosensoriel deafness, responding in varying degrees to thiamine treatment.

Aim: Report an unusual case of this rare disorder

Case Report: We report the case of a four-year-old boy who presented unusual features of thiamine-responsive megaloblastic anemia. In addition to the typical triad of the syndrome, he presented leuconeutropenia, hepatosplenomegalia, cardiac abnormalities including absent P waves, mitral and tricuspid insufficiency, retinitis pigmentosa, nystagmus, developmental delay and a brain Magnetic resonance imaging ischemic lesion.

Abundant extracellular myelin in the meninges of patients with multiple sclerosis.

Background: In multiple sclerosis (MS) myelin debris has been observed within MS lesions, in cerebrospinal fluid and cervical lymph nodes, but the route of myelin transport out of the brain is unknown. Drainage of interstitial fluid from the brain parenchyma involves the perivascular spaces and leptomeninges, but the presence of myelin debris in these compartments has not been described.

Aims: To determine whether myelin products are present in the meninges and perivascular spaces of MS patients.

Preactive lesions in multiple sclerosis.

Purpose Of Review: Knowledge of the early pathological changes observed in multiple sclerosis (MS) has advanced by implementation of many improved pathological, biochemical and imaging techniques. This review highlights the accumulating evidence for early pathological changes we term 'preactive lesions', characterized by clusters of activated microglia in otherwise normal-appearing white matter.

Recent Findings: Compelling evidence is accumulating for pathological changes in normal-appearing white matter of MS patients, which occur before the actual development of the active demyelinating lesion.

Gray matter pathology in (chronic) MS: modern views on an early observation.

Involvement of the gray matter (GM) in the pathology of multiple sclerosis (MS) was already recognized in the early days of MS research, but the detection of (cortical) GM lesions under the microscope and with magnetic resonance imaging (MRI) techniques was initially suboptimal and could only recently be enhanced. The visualization of GM lesions in vivo opens new doors for studies focusing on clinical, especially cognitive, effects of GM pathology, as well as for monitoring of neuroprotective treatment. However, so far little is known about what causes GM pathology.

T-cell responses to neurofilament light protein are part of the normal immune repertoire.

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system in which axonal damage and degeneration contribute significantly to the progressive irreversible neurological disability. Similar to pathogenic myelin autoimmunity, autoimmune responses to neuronal antigens may contribute to axonal damage and irreversible disability in MS. Auto-antibodies to the axonal cytoskeletal protein neurofilament light (NF-L) are associated with cerebral atrophy in MS and we have recently reported that NF-L autoimmunity is pathogenic in mice.

The phlebotomine fauna (Diptera: Psychodidae) of the eastern coast of Tunisia.

To identify the phlebotomine sand fly populations of the eastern coast of Tunisia, an entomological survey was carried out between September and October 2005 at 71 sites located in three districts. CDC light traps and sticky papers were used to collect a total of 2,138 phlebotomine sand flies representing nine species. The predominant species occurring on the eastern coast of Tunisia are, in order of abundance, Phlebotomus longicuspis Nitzulescu, 1930 (40%); Phlebotomus papatasi Scopoli, 1786 (21%); Sergentomyia minuta Parroti Adler & Theodor, 1927 (19%); Phlebotomus perniciosus Newstead, 1911 (9.

Brain antigens in functionally distinct antigen-presenting cell populations in cervical lymph nodes in MS and EAE.

Drainage of central nervous system (CNS) antigens to the brain-draining cervical lymph nodes (CLN) is likely crucial in the initiation and control of autoimmune responses during multiple sclerosis (MS). We demonstrate neuronal antigens within CLN of MS patients. In monkeys and mice with experimental autoimmune encephalomyelitis (EAE) and in mouse models with non-inflammatory CNS damage, the type and extent of CNS damage was associated with the frequencies of CNS antigens within the cervical lymph nodes.

Surgical excision of CNS-draining lymph nodes reduces relapse severity in chronic-relapsing experimental autoimmune encephalomyelitis.

Despite lack of classical lymphatic vessels in the central nervous system (CNS), cells and antigens do reach the CNS-draining lymph nodes. These lymph nodes are specialized to mediate mucosal immune tolerance, but can also generate T- and B-cell immunity. Their role in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) therefore remains elusive.

Axonal loss and gray matter pathology as a direct result of autoimmunity to neurofilaments.

Axonal damage is considered the major cause of irreversible disability in multiple sclerosis (MS). Which mechanisms underlie the damage and whether this is secondary to myelin damage remains to be clarified. Recently, we have demonstrated that autoimmunity to the axonal/neuronal cytoskeletal protein neurofilament light (NF-L) induces axonal damage and neurological disease including spasticity - a common feature of MS.

Targeting the tetraspanin CD81 blocks monocyte transmigration and ameliorates EAE.

Leukocyte infiltration is a key step in the development of demyelinating lesions in multiple sclerosis (MS), and molecules mediating leukocyte-endothelial interactions represent prime candidates for the development of therapeutic strategies. Here we studied the effects of blocking the integrin-associated tetraspanin CD81 in in vitro and in vivo models for MS. In an in vitro setting mAb against CD81 significantly reduced monocyte transmigration across brain endothelial cell monolayers, both in rodent and human models.

Oligodendrocyte-specific protein is encephalitogenic in rhesus macaques and induces specific demyelination of the optic nerve.

Oligodendrocyte-specific protein (OSP) is a candidate autoantigen in the development of multiple sclerosis (MS). We evaluated the potential of OSP to induce EAE in rhesus monkeys, an out bred animal model for MS that is immunologically close to humans. Since OSP is a four-membrane spanning protein with highly hydrophobic regions, we synthesized recombinant proteins encompassing only the hydrophilic regions of human OSP (soluble (s)hOSP).

[Retinal neovascularization with myelinated nerve fibers].

Introduction: The prevalence of myelinated retinal nerve fibers is 0.3%-0.6% of eyes.

Autoimmunity against myelin oligodendrocyte glycoprotein is dispensable for the initiation although essential for the progression of chronic encephalomyelitis in common marmosets.

To elucidate the pathogenetic significance of myelin/oligodendrocyte glycoprotein (MOG)-specific autoreactivity in a genetically and immunologically heterogeneous nonhuman primate model of multiple sclerosis, we analyzed experimental autoimmune encephalomyelitis (EAE) in the outbred common marmoset (Callithrix jacchus). One sibling each of 5 bone marrow chimeric marmoset twins was immunized with myelin derived from wild-type (WT) C57BL/6 mice (WT myelin); the other sibling was immunized with myelin from MOG-deficient C57BL/6 mice (MOG -/- myelin). One twin pair developed acute EAE simultaneously; the 4 remaining twin siblings immunized with WT myelin developed chronic progressive EAE, whereas siblings of these 4 monkeys remained free of clinical disease signs.

Resistance is futile: antineuronal autoimmunity in multiple sclerosis.

For many years, loss of myelin was considered to be the major cause of neurological dysfunction in multiple sclerosis (MS), a chronic inflammatory, demyelinating disease of the central nervous system. This 'myelinocentric' view of MS was revised recently, after recognition that axonal damage, rather than demyelination, provides a better correlate to clinical symptoms. Nonetheless, current views of MS pathogenesis remain focused on the role of myelin-specific autoimmunity, and the potential contribution of autoimmune responses to axonal and neuronal antigens is ignored.

[Cardiotoxicity of n-methyl-glucamine antimoniate (Glucantime). A case report].

The pentavalent antimonial meglumine (Glucantime) is the drug of choice in treatment of cutaneous leishmaniasis in Tunisia. It may create severe adverse effects. A ten year-old girl was treated by Glucantime for cutaneous leishmaniasis.

Epidemiology and risk factors for corneal graft rejection.

Objective: The aim of this study was to evaluate the frequency and main risk factors for corneal graft rejection.

Patients And Methods: This retrospective study included 285 eyes in 256 patients who underwent a penetrating keratoplasty (KPT) from January 1995 to December 2004. The minimum follow-up was 12 months to evaluate graft evolution.

[Keratoplasy for Peters anomaly (clinical case)].

Introduction: Peters anomaly is a primitive congenital glaucoma characterised by a central corneal leukoma. Therefore, keratoplasty is essential in addition to the specific treatment of the glaucoma. We aim to study the particularities and the evolutional ways of penetrating keratoplasty in Peters anomaly by presenting a clinical case treated in our service.

Differentiation of primary adult microglia alters their response to TLR8-mediated activation but not their capacity as APC.

Activated microglia are found in a variety of neuroinflammatory disorders where they have attributed roles as effector as well as antigen-presenting cells (APC). Critical determinants for the multifaceted role of microglia are the differentiation potential of microglia and their mode of activation. In this study, we have investigated the effects of M-CSF and GM-CSF-mediated differentiation of adult primate microglia on their cellular phenotype, antigen presentation, and phagocytic function as well as on Toll-like receptor (TLR)-mediated responses.