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| Previous Nomenclature | stem body, midbody |
| Description | Staining of the intercellular bridge that connects daughter cells by the end of cell division, but before cell separation. |
| Antigen Association | none |
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Clinical Relevance
First level information About Clinical Relevance & List of Abbreviations |
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▶ The AC-27 pattern has low positive predictive value for any disease (116) ▶ Found very infrequently in a routine serology diagnostic setting (117) ▶ Antigens recognized include, among other, CENP-E, CENP-F, TD60, MSA36, KIF-14, MKLP-1, MPP1/KIF20B, and INCENP; specific immunoassays for these autoantibodies are currently not commercially available (116, 118, 119) |
| First level information references |
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116. Rattner JB, Mack GJ, Fritzler MJ. Autoantibodies to components of the mitotic apparatus. Mol Biol Rep 1998;25:143-55. 117. Vermeersch P, Bossuyt X. Prevalence and clinical significance of rare antinuclear antibody patterns. Autoimmun Rev 2013;12:998-1003. 118. Humbel RLConrad K, ed. Autoantibodies to mitotic cells. In Dresden autoantibody symposium. Dresden Germany: Pabst Science, 2013: 327-39. 119. Rodriguez-Bayona B, Ruchaud S, Rodriguez C, et al. Autoantibodies against the chromosomal passenger protein INCENP found in a patient with Graham Little-Piccardi-Lassueur syndrome. J Autoimmune Dis 2007;4. |
| Second level information |
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▶ Incidentally described in patients with SSc, Raynaud’s phenomenon, and malignancy (10-12) ▶ Autoantibodies to CENP-E, CENP-F, TD60, MSA36, KIF-14, and MKLP-1 have been described in patients with SSc (limited and diffuse), SLE, and malignancies (13, 14) ▶ Autoantibodies to INCENP have been described in a single patient with Graham-Little-Piccardi-Lasseur Syndrome (15) ▶ Autoantibodies to MPP1 /KIF20B (M-phase phosphoprotein 1) have been described in patients with idiopathic ataxia, other neurological syndromes and paroxysmal nocturnal haemoglobinuria (16, 17) Notes: Most reports describe autoantibodies directly binding to specific antigens (i.e., antigen-specific immunoassays) and do not actually show correlations with the AC-27 pattern as such; specific immunoassays for these autoantibodies are currently not commercially available. |
| Second level information references |
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10. Fritzler MJ, Ayer LM, Gohill J, et al. An antigen in metaphase chromatin and the midbody of mammalian cells binds to scleroderma sera. J Rheumatol 1987;14:291-4. 11. Tausche AK, Conrad K, Seidel W, et al. Anti-midbody antibodies as a possible predictive factor for a special limited or abortive form of systemic sclerosis? Ann Rheum Dis 2005;64:1237-8. 12. Vermeersch P, Bossuyt X. Prevalence and clinical significance of rare antinuclear antibody patterns. Autoimmun Rev 2013;12:998-1003. 13. Rattner JB, Mack GJ, Fritzler MJ. Autoantibodies to components of the mitotic apparatus. Mol Biol Rep 1998;25:143-55. 14. Humbel RL. Autoantibodies to mitotic cells. in Dresden Autoantibody Symposium (eds. Conrad, K., et al.) 327-39 (Pabst Science, Dresden, Germany, 2013). 15. Rodriguez-Bayona B, Ruchaud S, Rodriguez C, et al. Autoantibodies against the chromosomal passenger protein INCENP found in a patient with Graham Little-Piccardi-Lassueur syndrome. J Autoimmune Dis 2007;4:1. 16. Fritzler MJ, Kerfoot SM, Feasby TE, et al. Autoantibodies from patients with idiopathic ataxia bind to M-phase phosphoprotein 1 (MPP-1). J Invest Med 2000;48:28-39. 17. Alahmad A, Preuss KD, Schenk J, et al. Desmoplakin and KIF20B as target antigens in patients with paroxysmal nocturnal haemoglobinuria. Br J Haematol 2010;151:273-80. |
| FAQ |
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How to deal with just a “nuclear speckled” IFA report? In my practice I have followed patients with ANA findings, with a nuclear speckled pattern (without specifying whether fine/dense/coarse), in patients with very heterogeneous phenotypes, some with a clinical picture that suggests further investigation of systemic autoimmune disease (one patient with proximal muscle weakness and skin thickening) and others who represent only non-specific findings. In such situations, as a precaution, I request more specific autoantibodies. However, this pattern (nuclear speckled pattern) is not described by the "ICAP" and I am in doubt about which antigenic association it represents, even to guide which autoantibody may be present and which ones to look after. How to interpret this pattern? Does the lab describe it when it is not possible to "refine" such a conclusion? Could this be associated with deficiency in the methodology, sample, interpretation? |