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2362 Part XIII: Transfusion Medicine Chapter 137: Human Leukocyte and Platelet Antigens 2363
thrombocytopenic purpura. Phase III assays have an advantage over 5. Holdsworth R, Hurley CK, Marsh SG, et al: The HLA dictionary 2008: A summary of
141
both phase I and phase II tests in that they detect antibodies that bind HLA-A, -B, -C, DRB1/3/4/5, and DQB1 alleles and their association with serologically
defined HLA-A, -B, -C, -DR, -DQ antigens. Tissue Antigens 73:95, 2009.
to platelet GPs, and not to non–platelet-specific epitopes, such as class I 6. Horton R, Wilming L, Rand V, et al: Gene map of the extended human MHC. Nat Rev
HLA. Examples of phase III assays are the monoclonal antibody immo- Genet 5:889, 2004.
142
bilization of platelet antigens assay (MAIPA) and the modified anti- 7. Thorsby E: Structure and function of HLA molecules. Transplant Proc 19:29, 1987.
gen capture ELISA (MACE). 143 8. Le Bouteiller P: HLA class I chromosomal region, genes, and products: Facts and ques-
tions. Crit Rev Immunol 14:89, 1994.
Although most of the platelet antibody detection methods can be 9. Mueller-Eckhardt G, Hauck M, Kayser W, Mueller-Eckhardt C: HLA-C antigens on
employed to determine platelet alloantigen types of individuals, because platelets. Tissue Antigens 16:91, 1980.
of limited access to rare typing sera and the need to establish platelet 10. Bjorkman PJ, Saper MA, Samraoui B, et al: The foreign antigen binding site and T cell
recognition regions of class I histocompatibility antigens. Nature 329:512, 1987.
typing in patients with very few platelets, they have been largely sup- 11. Campbell RD, Trowsdale J: Map of the human MHC. Immunol Today 14:349, 1993.
planted by molecular typing using methods based on PCR. Molecular 12. Trowsdale J: Genetics and polymorphism: Class II antigens. Br Med Bull 43:15, 1987.
typing is now available for all of the platelet alloantigens that have been 13. Germain RN, Margulies DH: The biochemistry and cell biology of antigen processing
and presentation. Annu Rev Immunol 11:403, 1993.
elucidated at the gene level. 144–150 14. Yewdell JW, Bennink JR: The binary logic of antigen processing and presentation to T
cells. Cell 62:203, 1990.
CLINICAL IMPORTANCE 15. Vyas JM, Van der Veen AG, Ploegh HL: The known unknowns of antigen processing
and presentation. Nat Rev Immunol 8:607, 2008.
Antibodies recognizing platelet-specific alloantigens have been discov- 16. Boon T, Coulie PG, Van den Eynde BJ, van der Bruggen P: Human T cell responses
against melanoma. Annu Rev Immunol 24:175, 2006.
ered in three clinical situations: mothers who give birth to infants with 17. Marsh SG; WHO Nomenclature Committee for Factors of the HLA System: Nomencla-
FNAIT; patients who develop dramatic thrombocytopenia after blood ture for factors of the HLA system, update April 2010. Tissue Antigens 76: 501, 2010.
transfusion (PTP); and patients who have received multiple transfu- 18. Cao K, Hollenbach J, Shi X, et al: Analysis of the frequencies of HLA-A, B, and C alleles
sions. Chapter 117 discusses the clinical syndromes of FNAIT. and haplotypes in the five major ethnic groups of the United States reveals high levels of
Although antibodies to class I HLA antigens are the principal diversity in these loci and contrasting distribution patterns in these populations. Hum
Immunol 62:1009, 2001.
cause of immunologic platelet transfusion refractoriness (discussed in 19. Maiers M, Gragert L, Klitz W: High-resolution HLA alleles and haplotypes in the
Chap. 139), occasionally patients receiving multiple platelet transfusions United States population. Hum Immunol 68:779, 2007.
will develop antibodies to platelet specific alloantigens. Many of the 20. Terasaki PI, Park MS, Bernoco D, Iwaki Y: Serology of HLA. Transplant Proc 13:900, 1981.
21. Terasaki PI, McClelland JD: Microdroplet assay of human serum cytotoxins. Nature
best-documented platelet-specific antibodies detected in such patients 204:998, 1964.
are directed against platelet antigens whose phenotypic frequencies are 22. Saiki RK, Gelfand DH, Stoffel S, et al: Primer-directed enzymatic amplification of DNA
less than 30 percent in the blood-donor population. 151–154 Therefore, it with a thermostable DNA polymerase. Science 239:487, 1988.
is difficult to attribute refractory responses in random-donor and/or 23. Schaffer M, Olerup O: HLA-AB typing by polymerase-chain reaction with sequence-
specific primers: More accurate, less errors, and increased resolution compared to sero-
HLA-matched platelet transfusions to these antibodies alone. Indeed, logical typing. Tissue Antigens 58:299, 2001.
the majority of refractory patients with platelet-specific antibodies also 24. Tait BD, Süsal C, Gebel HM, et al: Consensus guidelines on the testing and clinical
have HLA antibodies. Alloimmunization to high-frequency platelet- management issues associated with HLA and non-HLA antibodies in transplantation.
Transplantation 95:19, 2013.
specific antigens would be expected to present a major challenge in 25. O’Leary JG, Michelle Shiller S, Bellamy C, et al: Acute liver allograft antibody-mediated
finding compatible platelets to support a patient requiring multiple rejection: An inter-institutional study of significant histopathological features. Liver
Transpl 20:1244, 2014.
platelet transfusions. Fortunately, these cases are extremely rare. 152,154 26. Flomenberg N, Baxter-Lowe LA, Confer D, et al: Impact of HLA class I and class II
If platelet transfusion refractoriness does develop because of platelet- high-resolution matching on outcomes of unrelated donor bone marrow transplanta-
specific antibodies, compatible platelet products may be identified by tion: HLA-C mismatching is associated with a strong adverse effect on transplantation
using either platelet crossmatching or by accessing family member outcome. Blood 104:1923, 2004.
or other HPA-typed donors who are compatible with the patient’s 27. Petersdorf EW, Gooley T, Malkki M, Horowitz M: Clinical significance of donor-
recipient HLA matching on survival after myeloablative hematopoietic cell transplanta-
antibodies. 155,156 Platelet GP reactivity in transfusion recipients that lacks tion from unrelated donors. Tissue Antigens 69 Suppl 1:25, 2007.
specificity usually does not influence transfusion responses. 151,157–159 28. Bowness P: HLA and the spondyloarthropathies, in HLA in Health and Disease, 2nd ed,
edited by A Warrens, R Lechler, p 187. Academic Press, London, 2000.
Antibodies against some HPA-allelic determinants can inhibit 29. Sollid L, Spurkland A, Thorsby T: HLA and gastrointestinal diseases, in HLA in Health
platelet function. Anti–HPA-1 alloantibodies, for example, can inhibit and Disease, 2nd ed, edited by A Warrens, R Lechler, p 249. Academic Press, London,
clot retraction and platelet aggregation, presumably because they block 2000.
the binding of GPIIb/IIIa (α β ) (CD41/CD61) to fibrinogen. More- 30. Riley JP, Rosenberg SA, Parkhurst MR: Identification of a new shared HLA-A2.1
restricted epitope from the melanoma antigen tyrosinase. J Immunother 24:212, 2001.
IIb 3
over, anti–HPA-4 alloantibodies can completely inhibit aggregation of 31. Rezvani K, Yong AS, Mielke S, et al: Leukemia-associated antigen-specific T-cell
HPA-4 platelets that are homozygous for the allele recognized by the responses following combined PR1 and WT1 peptide vaccination in patients with mye-
alloantibodies because the epitope is in close proximity to the RGD loid malignancies. Blood 111:236, 2008.
(arginine-glycine-aspartic acid peptide sequence)-binding domain of 32. Abel S, Paturel L, Cabie A: Abacavir hypersensitivity. N Engl J Med 358:2515, 2008.
33. Bux J: Nomenclature of neutrophil alloantigens. ISBT Working Party on Platelet and
the α β integrin. 160,161 On the other hand, other anti–HPA-alloanti- Neutrophil Serology, Neutrophil Antigen Working Party. International Society of Blood
IIb 3
bodies, such as those specific for HPA-3, may not significantly interfere Transfusion. Transfusion 39:662, 1999.
with platelet function but nonetheless can cause Fc-mediated platelet 34. Bux J, Stein EL, Bierling P, et al: Characterization of a new alloantigen (SH) on the
human neutrophil Fc gamma receptor IIIb. Blood 89:1027, 1997.
destruction and immune thrombocytopenia. 162 35. Trounstine ML, Peltz GA, Yssel H, et al: Reactivity of cloned, expressed human Fc
gamma RIII isoforms with monoclonal antibodies which distinguish cell-type-specific
and allelic forms of Fc gamma RIII. Int Immunol 2:303, 1990.
REFERENCES 36. Ory PA, Clark MR, Kwoh EE, et al: Sequences of complementary DNAs that encode
the NA1 and NA2 forms of Fc receptor III on human neutrophils. J Clin Invest 84:1688,
1989.
1. Breuning MH, van den Berg-Loonen EM, Bernini LF, et al: Localization of HLA on the 37. Ravetch JV, Perussia B: Alternative membrane forms of Fc gamma RIII(CD16) on
short arm of chromosome 6. Hum Genet 37:131, 1977. human natural killer cells and neutrophils. Cell type-specific expression of two genes
2. Complete sequence and gene map of a human major histocompatibility complex. The that differ in single nucleotide substitutions. J Exp Med 170:481, 1989.
MHC sequencing consortium. Nature 401:921, 1999. 38. Huizinga TW, Kleijer M, Tetteroo PA, et al: Biallelic neutrophil Na-antigen system is
3. Berrih S, Arenzana-Seisdedos F, Cohen S, et al: Interferon-gamma modulates HLA class II associated with a polymorphism on the phospho-inositol-linked Fc gamma receptor III
antigen expression on cultured human thymic epithelial cells. J Immunol 135:1165, 1985. (CD16). Blood 75:213, 1990.
4. Robinson J, Waller MJ, Parham P, et al: IMGT/HLA and IMGT/MHC: Sequence data- 39. Stroncek DF, Shankar R, Litz C, Clement L: The expression of the NB1 antigen on mye-
bases for the study of the major histocompatibility complex. Nucleic Acids Res 31:311, loid precursors and neutrophils from children and umbilical cords. Transfus Med 8:119,
2003. 1998.
Kaushansky_chapter 137_p2353-2364.indd 2362 9/21/15 3:50 PM

