Detection of annexin A8 antibodies in serum of patients with antiphospholipid syndrome

Scholz, Philipp; Auler, Markus; Ruthard, Johannes; Brachvogel, Bent; Klatt, Andreas R.; Streichert, Thomas

doi:10.11613/bm.2018.030703

Cited by 1 publication

(2 citation statements)

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“…Although the major cellular activities of annexin proteins are internal to cells, several annexins have been observed externally in free form and complexed with phospholipid entities, but whether this external presence is responsible for production of anti-annexin autoantibodies in patients remains unclear. Nevertheless, production of anti-annexin autoantibodies have been proposed to enhance the vulnerability for inflammation and autoimmune disorders by interfering with annexins’ ability to regulate apoptosis [ 37 , 38 , 39 , 40 , 41 , 42 , 43 ]. In this sense, it is interesting to note that both NOD/Shi and C57BL/6.NOD- Aec1Aec2 mice have increased levels of cellular apoptosis in the salivary and lacrimal glands prior to onset of clinical SS pathology [ 46 , 51 ].…”

Section: Discussionmentioning

confidence: 99%

“…Multiple studies have reported associations between annexins and autoimmune/auto-inflammatory pathologies [ 25 , 26 , 29 , 31 , 32 , 33 , 34 , 35 , 36 ], including the development of anti-annexin autoantibodies [ 37 , 38 , 39 , 40 , 41 , 42 , 43 ], but especially toward Anxa1, Anxa2, Anxa5, Anxa7, and Anxa11. Both over- and under-expressions of annexins are found in development and organ systems as well as pathological conditions ranging from cancers to auto-immune diseases, especially Rheumatoid arthritis (RA), Systemic lupus erythematosus (SLE), and Sjögren’s syndrome (SS).…”

Section: Introductionmentioning

confidence: 99%

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A Temporal Comparative RNA Transcriptome Profile of the Annexin Gene Family in the Salivary versus Lacrimal Glands of the Sjögren’s Syndrome-Susceptible C57BL/6.NOD-Aec1Aec2 Mouse

Peck

Ambrus

2022

IJMS

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A generally accepted hypothesis for the initial activation of an immune or autoimmune response argues that alarmins are released from injured, dying and/or activated immune cells, and these products complex with receptors that activate signal transduction pathways and recruit immune cells to the site of injury where the recruited cells are stimulated to initiate immune and/or cellular repair responses. While there are multiple diverse families of alarmins such as interleukins (IL), heat-shock proteins (HSP), Toll-like receptors (TLR), plus individual molecular entities such as Galectin-3, Calreticulin, Thymosin, alpha-Defensin-1, RAGE, and Interferon-1, one phylogenetically conserved family are the Annexin proteins known to promote an extensive range of biomolecular and cellular products that can directly and indirectly regulate inflammation and immune activities. For the present report, we examined the temporal expression profiles of the 12 mammalian annexin genes (Anxa1-11 and Anxa13), applying our temporal genome-wide transcriptome analyses of ex vivo salivary and lacrimal glands from our C57BL/6.NOD-Aec1Aec2 mouse model of Sjögren’s Syndrome (SS), a human autoimmune disease characterized primarily by severe dry mouth and dry eye symptoms. Results indicate that annexin genes Anax1-7 and -11 exhibited upregulated expressions and the initial timing for these upregulations occurred as early as 8 weeks of age and prior to any covert signs of a SS-like disease. While the profiles of the two glands were similar, they were not identical, suggesting the possibility that the SS-like disease may not be uniform in the two glands. Nevertheless, this early pre-clinical and concomitant upregulated expression of this specific set of alarmins within the immune-targeted organs represents a potential target for identifying the pre-clinical stage in human SS as well, a fact that would clearly impact future interventions and therapeutic strategies.

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