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Clinical and vaccine immunology : CVI2012; 19(7); 1054-1064; doi: 10.1128/CVI.00237-12

Fell Pony syndrome: characterization of developmental hematopoiesis failure and associated gene expression profiles.

Abstract: Fell Pony syndrome (FPS) is a fatal immunodeficiency that occurs in foals of the Fell Pony breed. Affected foals present with severe anemia, B cell lymphopenia, and opportunistic infections. Our objective was to conduct a prospective study of potential FPS-affected Fell Pony foals to establish clinical, immunological, and molecular parameters at birth and in the first few weeks of life. Complete blood counts, peripheral blood lymphocyte phenotyping, and serum immunoglobulin concentrations were determined for 3 FPS-affected foals, 49 unaffected foals, and 6 adult horses. In addition, cytology of bone marrow aspirates was performed sequentially in a subset of foals. At birth, the FPS-affected foals were not noticeably ill and had hematocrit and circulating B cell counts comparable to those of unaffected foals; however, over 6 weeks, values for both parameters steadily declined. A bone marrow aspirate from a 3-week-old FPS-affected foal revealed erythroid hyperplasia and concurrent erythroid and myeloid dysplasia, which progressed to a severe erythroid hypoplasia at 5 weeks of life. Immunohistochemical staining confirmed the paucity of B cells in primary and secondary lymphoid tissues. The mRNA expression of genes involved in B cell development, signaling, and maturation was investigated using qualitative and quantitative reverse transcriptase PCR (RT-PCR). Several genes, including CREB1, EP300, MYB, PAX5, and SPI1/PU.1, were sequenced from FPS-affected and unaffected foals. Our study presents evidence of fetal erythrocyte and B cell hematopoiesis with rapid postnatal development of anemia and B lymphopenia in FPS-affected foals. The transition between fetal/neonatal and adult-like hematopoiesis may be an important aspect of the pathogenesis of FPS.
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Publication Date: 2012-05-16 PubMed ID: 22593239PubMed Central: PMC3393361DOI: 10.1128/CVI.00237-12Google Scholar: Lookup
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  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research study investigates Fell Pony Syndrome, a fatal immunodeficiency in the Fell Pony breed, identifying the clinical, immunological and molecular parameters at birth and during the first few weeks of life. The research further compares these parameters with unaffected foals and full-grown adult horses to identify abnormalities.

Objective of the Research

  • The main objective of the study was a thorough characterization of Fell Pony Syndrome (FPS) to identify clinical, immunological, and molecular indicators of the disease at different stages of life in affected foals.

Methodology and Participants

  • The study included three FPS-affected foals, forty-nine unaffected foals and six adult horses.
  • Participants were subjected to a range of tests, including blood counts, peripheral blood lymphocyte phenotyping, serum immunoglobulin concentrations, and cytology of bone marrow aspirates.

Key Findings

  • Foals affected by FPS appeared healthy at birth, with blood cell counts similar to unaffected foals. However, both hematocrit and B cell counts declined over the course of 6 weeks.
  • Bone marrow analysis of a 3-week-old FPS-affected foal showed erythroid hyperplasia and concurrent erythroid and myeloid dysplasia. By the time the foal was 5 weeks old, erythroid hypoplasia had set in.
  • Immunohistochemical staining confirmed a deficiency of B cells in primary and secondary lymphoid tissues.
  • The study also examined the expression of certain genes, including CREB1, EP300, MYB, PAX5, and SPI1/PU.1, involved in B cell development, signalling, and maturation.

Conclusion

  • The study concluded that in FPS-affected foals, there is evidence of fetal erythrocyte and B cell hematopoiesis with rapid postnatal development of anemia and B lymphopenia.
  • It was suggested that the transitional phase from fetal/neonatal to adult-like hematopoiesis might be an essential aspect of FPS pathogenesis.

Cite This Article

APA
Tallmadge RL, Stokol T, Gould-Earley MJ, Earley E, Secor EJ, Matychak MB, Felippe MJ. (2012). Fell Pony syndrome: characterization of developmental hematopoiesis failure and associated gene expression profiles. Clin Vaccine Immunol, 19(7), 1054-1064. https://doi.org/10.1128/CVI.00237-12

Publication

Clinical and vaccine immunology : CVI
ISSN: 1556-679X
NlmUniqueID: 101252125
Country: United States
Language: English
Volume: 19
Issue: 7
Pages: 1054-1064

Researcher Affiliations

Tallmadge, Rebecca L
  • Departments of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.
Stokol, Tracy
    Gould-Earley, Mary Jean
      Earley, Ed
        Secor, Erica J
          Matychak, Mary Beth
            Felippe, M Julia B

              MeSH Terms

              • Anemia / congenital
              • Anemia / pathology
              • Anemia / veterinary
              • Animals
              • B-Lymphocytes / immunology
              • Bone Marrow / pathology
              • Gene Expression Profiling
              • Hematocrit
              • Hematopoiesis
              • Horse Diseases / congenital
              • Horse Diseases / pathology
              • Horses
              • Hyperplasia
              • Immunohistochemistry
              • Immunologic Deficiency Syndromes / congenital
              • Immunologic Deficiency Syndromes / pathology
              • Immunologic Deficiency Syndromes / veterinary
              • Lymphocyte Count
              • Prospective Studies
              • Time Factors

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              Citations

              This article has been cited 2 times.
              1. Badial PR, Tallmadge RL, Miller S, Stokol T, Richards K, Borges AS, Felippe MJ. Applied Protein and Molecular Techniques for Characterization of B Cell Neoplasms in Horses. Clin Vaccine Immunol 2015 Nov;22(11):1133-45.
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              2. Kasper LH, Fukuyama T, Lerach S, Chang Y, Xu W, Wu S, Boyd KL, Brindle PK. Genetic interaction between mutations in c-Myb and the KIX domains of CBP and p300 affects multiple blood cell lineages and influences both gene activation and repression. PLoS One 2013;8(12):e82684.
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