Phenotypic Identification Of Spinal Cord-Infiltrating CD4+ T Lymphocytes In A Murine Model Of Neuropathic Pain

Ks, Draleau; Maddula, Swathi; Slaiby, Aaron M.; Nutile-McMenemy, Nancy; Ja, De Leo; Cao, Lu

doi:10.4172/2167-0846.s3-003

Cited by 36 publications

(19 citation statements)

References 37 publications

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“…Animal studies have enlightened the role of T cells in pain development. In particular, the depletion of CD4 + T cells in a mouse model was able to inhibit thermal hyperalgesia and tactile central sensitization following partial sciatic nerve ligation [57,58].…”

Section: Role Of T Cells In Fibromyalgia: Literature Datamentioning

confidence: 99%

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

Banfi

Diani

Pigatto

et al. 2020

IJMS

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Fibromyalgia is one of the most important "rheumatic" disorders, after osteoarthritis. The etiology of the disease is still not clear. At the moment, the most defined pathological mechanism is the alteration of central pain pathways, and emotional conditions can trigger or worsen symptoms. Increasing evidence supports the role of mast cells in maintaining pain conditions such as musculoskeletal pain and central sensitization. Importantly, mast cells can mediate microglia activation through the production of proinflammatory cytokines such as IL-1β, IL-6, and TNFα. In addition, levels of chemokines and proinflammatory cytokines are enhanced in serum and could contribute to inflammation at systemic level. Despite the well-characterized relationship between the nervous system and inflammation, the mechanism that links the different pathological features of fibromyalgia, including stress-related manifestations, central sensitization, and dysregulation of the innate and adaptive immune responses is largely unknown. This review aims to provide an overview of the current understanding of the role of adaptive immune cells, in particular T cells, in the physiopathology of fibromyalgia. It also aims at linking the latest advances emerging from basic science to envisage new perspectives to explain the role of T cells in interconnecting the psychological, neurological, and inflammatory symptoms of fibromyalgia.

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Section: Role Of T Cells In Fibromyalgia: Literature Datamentioning

confidence: 99%

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

Banfi

Diani

Pigatto

et al. 2020

IJMS

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“…In addition to macrophages, T cells may also be important in the mechanisms that underlie pathological pain. For instance, activated CD4 + T cells, specifically Th1 and Th17 cells, migrate to associated lumbar DRG and/or the lumbar spinal cord dorsal horn in animal models of sciatic nerve transection (47)(48)(49), spared nerve injury (50,51), partial sciatic nerve ligation (52,53), and sciatic nerve chronic constriction injury (54).…”

Section: T Cells In Pathological Painmentioning

confidence: 99%

Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management

2019

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Current pain therapeutics offer inadequate relief to patients with chronic pain. A growing literature supports that pro-inflammatory cytokine signaling between immune, glial, and neural cells is integral to the development of pathological pain. Modulation of these communications may hold the key to improved pain management. In this review we first offer an overview of the relationships between pro-inflammatory cytokine and chemokine signaling and pathological pain, with a focus on the actions of cytokines and chemokines in communication between glia (astrocytes and microglia), immune cells (macrophages and T cells), and neurons. These interactions will be discussed in relation to both peripheral and central nervous system locations. Several novel non-neuronal drug targets for controlling pain are emerging as highly promising, including non-viral IL-10 gene therapy, which offer the potential for substantial pain relief through localized modulation of targeted cytokine pathways. Preclinical investigation of the mechanisms underlying the success of IL-10 gene therapy revealed the unexpected discovery of the powerful anti-nociceptive anti-inflammatory properties of D-mannose, an adjuvant in the non-viral gene therapeutic formulation. This review will include gene therapeutic approaches showing the most promise in controlling pro-inflammatory signaling via increased expression of anti-inflammatory cytokines like interleukin-10 (IL-10) or IL-4, or by directly limiting the bioavailability of specific pro-inflammatory cytokines, as with tumor necrosis factor (TNF) by the TNF soluble receptor (TNFSR). Approaches that increase endogenous anti-inflammatory signaling may offer additional opportunities for pain therapeutic development in patients not candidates for gene therapy. Promising novel avenues discussed here include the disruption of lymphocyte function-associated antigen (LFA-1) activity, antagonism at the cannabinoid 2 receptor (CB2R), and toll-like receptor 4 (TLR4) antagonism. Given the partial efficacy of current drugs, new strategies to manipulate neuroimmune and cytokine interactions hold considerable promise.

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“…They found that neuropathic pain is mediated by Th1 cells. 73 A recent experiment demonstrated that T cells infiltrate the dorsal root ganglion following peripheral nerve injury. Once in the dorsal root ganglion, they release leukocyte elastase, a proteinase that destroys bacteria and which has been linked to chronic inflammation.…”

Section: Immune Cell Involvement In Painmentioning

confidence: 99%

Immune system involvement in specific pain conditions

2017

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Chronic pain is a significant problem worldwide and is the most common disability in the United States. It is well known that the immune system plays a critical role in the development and maintenance of many chronic pain conditions. The involvement of the immune system can be through the release of autoantibodies, in the case of rheumatoid arthritis, or via cytokines, chemokines, and other inflammatory mediators (i.e. substance P, histamine, bradykinin, tumor necrosis factor, interleukins, and prostaglandins). Immune cells, such as T cells, B cells and their antibodies, and microglia are clearly key players in immune-related pain. The purpose of this review is to briefly discuss the immune system involvement in pain and to outline how it relates to rheumatoid arthritis, osteoarthritis, fibromyalgia, complex regional pain syndrome, multiple sclerosis, and diabetic neuropathy. The immune system plays a major role in many debilitating chronic pain conditions and we believe that animal models of disease and their treatments should be more directly focused on these interactions.

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Phenotypic Identification Of Spinal Cord-Infiltrating CD4+ T Lymphocytes In A Murine Model Of Neuropathic Pain

Cited by 36 publications

References 37 publications

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

T Cell Subpopulations in the Physiopathology of Fibromyalgia: Evidence and Perspectives

Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management

Immune system involvement in specific pain conditions

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