Late development of anti-La/SS-B antibodies in a patient with Sjogren's syndrome and high titer anti-Ro/SS-A antibodies

Satoh, Minoru; Hamilton, Kimberly J.; Langdon, J J; Akizuki, Masashi; Yamagata, H; Nakayama, Takeo; Wh, Reeves; Homma, Mitsuo

doi:10.1177/096120339600500417

Cited by 2 publications

(2 citation statements)

References 7 publications

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“…In unpredictable human diseases, such as SLE, autoantibodies can precede the onset of clinical symptomology by years [15,16]. Consequently, detecting the first human autoantibodies in any lupus autoimmune response is rare [17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Shared Early Autoantibody Recognition Events in the Development of Anti‐Sm B/B' in Human Lupus

Arbuckle¹,

Reichlin²,

Harley³

et al. 1999

Scand J Immunol

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Many aspects of the immune maturation are uncharted. For ordinary human autoimmune systems there are no complete descriptions of the progression from an initial antigenic epitope to a maximally complex immune response. In this study we have exploited a large serial collection of human sera to investigate the development of the anti-Sm autoimmune response in systemic lupus erythematosus (SLE). The results suggest a similar, if not virtually identical, stepwise progression in the early humoral immune maturation of anti-Sm. The amino acid sequence PPPGMRPP comprises the first epitope in the anti-Sm B/B'response and its close relative, PPPGMRGP, the second. Epitopes are subsequently enlarged by the incorporation of neighbouring amino acids. The third and fourth epitopes are also recognised by an antibody in a nearly identical sequence in different lupus patients. A column absorption with PPPGMRPP demonstrates that the epitope spreading among the first four early epitopes appears to occur by the sequential generation of cross-reactive antibodies. Unexpectedly, epitope spreading in this system occurs in a predictable fashion by involving essentially the same sequence of antigenic structures from person to person. In addition, these data support the lupus anti-Sm antibodies originating against a single antigenic structure and, hence, strongly support a unifying mechanism in the generation of these autoantibodies.

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Section: Introductionmentioning

confidence: 99%

Shared Early Autoantibody Recognition Events in the Development of Anti‐Sm B/B' in Human Lupus

Arbuckle¹,

Reichlin²,

Harley³

et al. 1999

Scand J Immunol

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“…Serologically negative SjD patients tend to be a stable group, in line with autoantibody profiles remaining stable over time ( 24 , 25 ); however, there are rare reports of patients who develop autoantibodies after diagnosis. For example, 1 patient with anti‐Ro autoantibodies and clinical evidence for SjD developed anti‐La several years after diagnosis ( 26 ). It is not clear whether this case reflects an increased production of anti‐La autoantibodies such that the titer reaches assay detection threshold or a spontaneous intermolecular spreading event, similar to that described in mice models ( 27 ).…”

Section: Pre‐diseasementioning

confidence: 99%

Phases and Natural History of Sjögren's Disease: A New Model for an Old Disease?

Lee

Wang

Gordon

et al. 2023

Arthritis Care & Research

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Sjögren's disease (SjD) is an archetypal and heterogenous autoimmune disorder that is characterized by exocrine glandular dysfunction. A proportion of patients develop severe extraglandular manifestations, such as cryoglobulinemia, and have an increased risk of lymphoma, both of which can adversely affect quality of life and occasionally mortality. As with most autoimmune disorders, the pathogenesis is poorly understood and difficult to predict, and, frustratingly, there is a lack of targeted therapies to cure this disease. We review the disease manifestations of SjD and propose a staged model for understanding the evolution of pathology. In longitudinal studies, most patients remain relatively stable in terms of their laboratory and clinical parameters. However, in the setting of various risk factors, a proportion of patients develop severe symptoms and/or lymphoma. We discuss potential underlying mechanisms for disease progression and the strengths and limitations of using a staged model to correlate the pathogenesis and spectrum of manifestations in SjD. Ultimately, understanding how and why some patients remain relatively stable, whereas others progress and develop florid systemic disease and a fraction develop lymphoma, is key to developing preventative and therapeutic treatments.

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Late development of anti-La/SS-B antibodies in a patient with Sjogren's syndrome and high titer anti-Ro/SS-A antibodies

Cited by 2 publications

References 7 publications

Shared Early Autoantibody Recognition Events in the Development of Anti‐Sm B/B' in Human Lupus

Shared Early Autoantibody Recognition Events in the Development of Anti‐Sm B/B' in Human Lupus

Phases and Natural History of Sjögren's Disease: A New Model for an Old Disease?

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