A naturally present autoantibody to senescent red blood cells?

Badior, Katherine E.; Bloch, Evgenia M.; Branch, Donald R.

doi:10.1111/trf.16883

Cited by 5 publications

(9 citation statements)

References 4 publications

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“…In contrast, patients with Type II wAIHA showed a lack of RBC aging, suggesting rapid and equal-opportunity opsonisation and the removal of RBCs [49], consistent with a previous report of Type II wAIHA being more severe than Type I wAIHA [44]. Additional investigations show that the natural autoantibody that binds to aged RBCs, indeed, recognizes band 3 [49,50]. Taken together, these findings generate the hypothesis that most wAIHA patients, at 80%, produce more of the senescent RBC autoantibody that reacts with patients' accelerated aging RBCs, for Type I wAIHA [42,49].…”

Section: Autoantibody Specificitysupporting

confidence: 89%

“…More recently, teams have shown that most warm autoantibodies do, in fact, target band 3 [42,49,50]. In a recent publication, the authors confirm Type I and Type II wAIHA and suggest that Type I wAIHA autoantibodies target band 3 and that the hemolytic anemia may conversely involve patient RBCs that are also aging faster than normal [48].…”

Section: Autoantibody Specificitymentioning

confidence: 97%

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Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management

Loriamini,

Cserti-Gazdewich,

Branch

2024

IJMS

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: Autoimmune hemolytic anemias (AIHAs) are conditions involving the production of antibodies against one’s own red blood cells (RBCs). These can be primary with unknown cause or secondary (by association with diseases or infections). There are several different categories of AIHAs recognized according to their features in the direct antiglobulin test (DAT). (1) Warm-antibody AIHA (wAIHA) exhibits a pan-reactive IgG autoantibody recognizing a portion of band 3 (wherein the DAT may be positive with IgG, C3d or both). Treatment involves glucocorticoids and steroid-sparing agents and may consider IVIG or monoclonal antibodies to CD20, CD38 or C1q. (2) Cold-antibody AIHA due to IgMs range from cold agglutinin syndrome (CAS) to cold agglutin disease (CAD). These are typically specific to the Ii blood group system, with the former (CAS) being polyclonal and the latter (CAD) being a more severe and monoclonal entity. The DAT in either case is positive only with C3d. Foundationally, the patient is kept warm, though treatment for significant complement-related outcomes may, therefore, capitalize on monoclonal options against C1q or C5. (3) Mixed AIHA, also called combined cold and warm AIHA, has a DAT positive for both IgG and C3d, with treatment approaches inclusive of those appropriate for wAIHA and cold AIHA. (4) Paroxysmal cold hemoglobinuria (PCH), also termed Donath–Landsteiner test-positive AIHA, has a DAT positive only for C3d, driven upstream by a biphasic cold-reactive IgG antibody recruiting complement. Although usually self-remitting, management may consider monoclonal antibodies to C1q or C5. (5) Direct antiglobulin test-negative AIHA (DAT-neg AIHA), due to IgG antibody below detection thresholds in the DAT, or by non-detected IgM or IgA antibodies, is managed as wAIHA. (6) Drug-induced immune hemolytic anemia (DIIHA) appears as wAIHA with DAT IgG and/or C3d. Some cases may resolve after ceasing the instigating drug. (7) Passenger lymphocyte syndrome, found after transplantation, is caused by B-cells transferred from an antigen-negative donor whose antibodies react with a recipient who produces antigen-positive RBCs. This comprehensive review will discuss in detail each of these AIHAs and provide information on diagnosis, pathophysiology and treatment modalities.

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Section: Autoantibody Specificitysupporting

confidence: 89%

Section: Autoantibody Specificitymentioning

confidence: 97%

Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management

Loriamini,

Cserti-Gazdewich,

Branch

2024

IJMS

Self Cite

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“…A recent letter to Transfusion by Badior et al has reported that IgG eluted from red blood cells (RBCs) of 20 blood donors binds to native degraded Band3, 1 supporting earlier elegant studies by the same group using X-ray crystallography that defined a discontinuous Band3 eptiope 2 as the target of antibodies to the senescent antigen (SA). The "SA hypothesis" is that, as RBCs age, molecular decay generates neo-epitopes (SA) and naturally occurring "autoantibodies" (anti-SA) then opsonize senescent RBCs, causing their clearance by the mononuclear phagocyte system.…”

mentioning

confidence: 73%

“…James C. Zimring 1,2 Steven L. Spitalnik 3 Krystalyn E. Hudson 3 1 Department of Pathology, University of Virginia School of…”

Section: Conflict Of Interestmentioning

confidence: 99%

The senescent antigen hypothesis of RBC evanescence: 50 years of correlation without causation

2022

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“…The current paradigm of RBC homeostasis is based on two main assumptions: EPO regulates the production of new cells in the bone marrow [15, 53], and sinusoidal macrophages remove RBCs from the blood when they attain a certain species-specific age [54]. Qualitatively, these elements seem to provide a sound explanation for the control of RBC populations.…”

Section: Discussionmentioning

confidence: 99%

Killing them softly with EPO: a new role for erythropoietin in the homeostasis of red blood cells

Arias

Valente-Leal

Bertocchini

et al. 2023

Preprint

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The regulation of red blood cell (RBC) homeostasis is widely assumed to rely on the control of cell production by erythropoietin (EPO) and the destruction of cells at a fixed, species-specific age. In this work, we show that such a regulatory mechanism is a poor homeostatic solution to satisfy the changing needs of the body. Effective homeostatic control requires RBC lifespan to be variable and tightly regulated. We show that EPO controls RBC lifespan by determining CD47 expression in newly formed RBCs and SIRP-α expression in sinusoidal macrophages. EPO also controls the initiation and intensity of anti-RBC autoimmune responses that curtail RBC lifespan in some circumstances. These mechanisms continuously modulate the rate of RBC destruction depending on oxygen availability. The finding of new homeostatic roles for EPO and autoimmunity critically challenges the current paradigm of RBC homeostasis and sets the grounds for a new approach to this field.

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A naturally present autoantibody to senescent red blood cells?

Cited by 5 publications

References 4 publications

Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management

Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management

The senescent antigen hypothesis of RBC evanescence: 50 years of correlation without causation

Killing them softly with EPO: a new role for erythropoietin in the homeostasis of red blood cells

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