ArticlePain2017
Passive transfer autoimmunity in a mouse model of complex regional pain syndrome.
Article in Pain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- The neuroimmune axis and chronic pain disorders.iScience · 2026Review
- Cellular and molecular changes in the skin driving increased nociception and pain during burn injury and repair.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Article
- Review
- New paradigms in pain management after skeletal trauma: Orthopaedic Trauma Association's 2023 Basic Science Focus Forum Symposium.OTA international : the open access journal of orthopaedic trauma · 2025Article
- Efficacy of Immunotherapy for Complex Regional Pain Syndrome: A Narrative Review.Current pain and headache reports · 2025Review
- Comprehensive Mechanisms and Non-Invasive Treatment for Complex Regional Pain Syndrome: A Narrative Review.Journal of pain research · 2025Review
- Autoantibodies cause nociceptive sensitization in a mouse model of degenerative osteoarthritis.Pain · 2024Article
- Review
- Effects of immunosuppression after limb fracture in mice on nociceptive, cognitive, and anxiety-related outcomes.Pain reports · 2024Article
- B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.Science translational medicine · 2024Article
- Mechanisms of complex regional pain syndrome.Frontiers in pain research (Lausanne, Switzerland) · 2024Review
- Microbiota-Accessible Boron-Containing Compounds in Complex Regional Pain Syndrome.Medicina (Kaunas, Lithuania) · 2023Review
- Pain-resolving immune mechanisms in neuropathic pain.Nature reviews. Neurology · 2023Review
- The autoimmune aetiology of unexplained chronic pain.Autoimmunity reviews · 2022Review
- Autonomic Regulation of Nociceptive and Immunologic Changes in a Mouse Model of Complex Regional Pain Syndrome.The journal of pain · 2022Article
- Sex-Specific B Cell and Anti-Myelin Autoantibody Response After Peripheral Nerve Injury.Frontiers in cellular neuroscience · 2022Article
- Potential Neuroimmune Interaction in Chronic Pain: A Review on Immune Cells in Peripheral and Central Sensitization.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- IL-6 signaling mediates the germinal center response, IgM production and nociceptive sensitization in male mice after tibia fracture.Brain, behavior, and immunity · 2021Article
- Animal Models of Complex Regional Pain Syndrome Type I.Journal of pain research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
It has been proposed that complex regional pain syndrome (CRPS) is a posttraumatic autoimmune disease, and we previously observed that B cells are required for the full expression of CRPS-like changes in a mouse tibia fracture CRPS model. The current study used the mouse model to evaluate the progression of postfracture CRPS-like changes in wild-type (WT) and muMT fracture mice lacking B cells and antibodies. The pronociceptive effects of injecting WT fracture mouse serum antibodies into muMT fracture mice were also evaluated. Postfracture pain behaviors transitioned from being initially dependent on both innate and autoimmune inflammatory mechanisms at 3 weeks after fracture to being entirely mediated by antibody responses at 12 weeks after fracture and spontaneously resolving by 21 weeks after fracture. Furthermore, serum IgM antibodies from WT fracture mice had pronociceptive effects in the fracture limb when injected into muMT fracture mice. IgM antibody levels gradually increased in the fracture limb hind paw skin, sciatic nerve, and corresponding lumbar cord, peaking at 12 to 18 weeks after fracture and then declining. Immunohistochemistry localized postfracture IgM antibody binding to antigens in the fracture limb hind paw dermal cell nuclei. We postulate that fracture induces expression of neoantigens in the fracture limb skin, sciatic nerve, and cord, which trigger B cells to secret IgM antibodies that bind those antigens and initiate a pronociceptive antibody response. Autoimmunity plays a key role in the progression of nociceptive and vascular changes in the mouse fracture model and potentially contributes to the CRPS disease process.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.