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viii Editors: Thiago Devesa Marquez and Davi Urgeiro Neto

importantly, RP105(-) B cells produce autoantibodies including anti-dsDNA antibodies.

RP105(-) B cells are assigned as the B cell subsets in final stages of differentiation and may
be one of the central B cells dysregulated in SLE. This review provides basic information of
B cell biology and RP105(-) B cells in SLE and illustrates new insights of novel and
alternative concept of B cell targeting therapies in SLE.
Chapter III - Systemic lupus erythematosus (SLE) is an autoimmune disorder that affects
0.1% of the world population. The disorder is characterized by systemic inflammation, auto-
antibody production, and immune dysregulation, and it may lead to significant neurological
and psychiatric morbidities. Both adults and children are diagnosed according to a set of
clinical and laboratory criteria with a high sensitivity and specificity. A diagnosis of SLE in
any age-group depends on excluding systemic infections or malignancies and the presence of
at least 4 of 11 American College of Rheumatology (ACR) diagnostic criteria. Nephritis
(leading to hypertension and renal dysfunction) and nervous system involvement are two of
the more ominous manifestations in all age-groups. There are 19 case-based peripheral and
central nervous syndromes that are postulated to be associated with SLE. Syndromes
requiring prompt neurological evaluation include seizures, cerebrovascular accidents,
demyelination, movement disorders, and peripheral neuropathies. Manifestations that may
prompt psychiatric consultation include acute confusional state (delirium), affective disorders
(anxiety and depression), cognitive impairment, and psychosis. Neuropsychiatric
presentations may be caused by hypercoagulability in cerebral vessels (vasculopathy),
proinflammatory cytokines, autoantibody effects on neuronal structures or receptors, and
bloodbrain barrier disruption. Alteration in the regulation of neurotransmitters such as
dopamine and serotonin appear to play a role in behavioral changes seen in lupus-prone mice.
The authors will review the prevalence, etiology and clinical presentation of neuropsychiatric
manifestations in SLE. In addition, we will discuss treatment protocol for this serious
manifestation in SLE.
Chapter IV - Systemic lupus erythematosus (SLE) is a prototypic inflammatory
autoimmune disorder characterized by multisystem involvement and fluctuating disease
activity. Symptoms range from rather mild manifestations such as rash or arthritis to life-
threatening end-organ manifestations such as nephritis. Despite new and improved therapy
having positively impacted the prognosis of SLE, a subgroup of patients do not response to
therapy. Moreover, the risk of fatal outcomes and the damaging side effects of
immunosuppressive therapies in SLE call for an improvement in the current therapeutic
management of SLE. New therapeutic approaches are focused on B-cell targets, T-cell
downregulation and co-stimulatory blockade, cytokine inhibition, or the modulation of
complement. Several biological agents have been used in recent and ongoing studies, but this
encouraging news follows several disappointments in trials of other biologic therapies. We
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will review potential therapeutics in SLE and reflect on where we stand, what we have
learned, and what may lie ahead.
Chapter V - A chronic disorder with unknown etiology, systemic lupus erythematosus
(SLE) is the most diverse autoimmune disorder with a relapsing and remitting course that
may affect any organ in the body. SLE has a broad spectrum of clinical presentations with
higher mortality than general population. These diverse clinical manifestations are mainly due
to SLE complex immunopathology in which B cells produce autoantibodies against mainly
intracellular auto antigen targets, and form complement fixing immune complex deposits
resulting in irreversible organ damage. More than one hundred autoantibodies have been

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