Immunophenotypic study of basophils by multiparameter flow cytometry.
Context.--The immunophenotypic profile of basophils is not yet
fully established, and the immunophenotypic changes in chronic
myelogenous leukemia are not fully characterized.
Objective.--To establish a comprehensive immunophenotypic spectrum of normal basophils and to assess the range of immunophenotypic aberrations of basophils in chronic myelogenous leukemia.
Design.--Using 4-color flow cytometry, we compared the immunophenotypic profile of basophils in peripheral blood or bone marrow samples from 20 patients with no evidence of neoplasia to basophils from 15 patients with chronic myelogenous leukemia.
Results.--Basophils in control cases were all positive for CD9, CD13, CD22, CD25 (dim), CD33, CD36, CD38 (bright), CD45 (dimmer than lymphocytes and brighter than myeloblasts), and CD123 (bright), and were negative for CD19, CD34, CD64, CD117, and HLA-DR. Basophils in all chronic myelogenous leukemia patients possessed 1 to 5 immunophenotypic aberrancies. The most common aberrancies were underexpression of CD38, followed by aberrant expression of CD64 and underexpression of CD123. CD34 and CD117 were present in cases with basophilic precursors. Myeloblasts showed a distinct immunophenotypic profile, as they typically expressed CD34 and CD117, showed dimmer expression (compared with basophils) of CD38, CD45, and CD123, and lacked expression of CD22.
Conclusions.--Flow cytometric immunophenotyping can identify immunophenotypic aberrations of basophils in chronic myelogenous leukemia, and discriminate basophils from myeloblasts.
Phenotype (Identification and classification)
Flow cytometry (Methods)
Parameter estimation (Methods)
Jorgensen, Jeffrey L.
Huh, Yang O.
|Publication:||Name: Archives of Pathology & Laboratory Medicine Publisher: College of American Pathologists Audience: Academic; Professional Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2008 College of American Pathologists ISSN: 1543-2165|
|Issue:||Date: May, 2008 Source Volume: 132 Source Issue: 5|
|Topic:||Event Code: 310 Science & research|
|Geographic:||Geographic Scope: United States Geographic Code: 1USA United States|
Basophils are the least common blood granulocytes, with a
prevalence of about 0.5% of total leukocytes and about 0.3% of nucleated
marrow cells in a healthy individual, (1,2) and acute basophilic
leukemia is very rare. (3) The immunophenotypic profile (IP) of
basophils thus has not previously been systematically analyzed. A
limited number of immunophenotypic studies by flow cytometry have
demonstrated that basophils show a [CD11b.sup.+]/
immunophenotype. (4,5) While basophil-associated markers have been
identified, such as immunoglobulin (Ig) E, CDw17, CD88, and FceRI, (6-8)
these markers are not routinely used in the clinical flow cytometry
laboratory. Additional markers, such as CD9, CD22, and CD123, reportedly
expressed on basophils, (2,4,6-11) are not commonly analyzed in
nonneoplastic or in most neoplastic conditions.
The basophil count is consistently increased in chronic myelogenous leukemia (CML), a type of chronic myeloproliferative disease caused by a clonal stem cell disorder. The disease is bi- or triphasic with an initial indolent chronic phase (CML-CP) that is followed by 1 or both of the aggressive transformed stages: accelerated phase (CML-AP) and/or blast phase (CML-BP). Both CML-AP and CML-BP are characterized by an increase in basophils and/or an increase in myeloblasts. (12) The basophils may not be easily identified in the smears because of frequent morphologic atypicality. In addition, as the patterns of CD45 expression and light scatter properties of basophils are similar to those of myeloblasts, this could potentially lead to an inaccurate overestimation of myeloblasts. Therefore, there is a need to identify the immunophenotypic spectrum of basophils by routinely used markers.
Multiparameter flow cytometric immunophenotyping has been increasingly applied to the diagnosis of myelodysplastic syndromes and chronic myeloproliferative diseases in recent years. (5,13-15) These studies have largely focused on the aberrant antigen expression on granulocytes and monocytes; less is known about the immunophenotypic aberrancies on basophils. In the present study, we compared the immunophenotypic features of basophils from control patients with no evidence of lymphoid/myeloid neoplasms to basophils from patients with CML. Our aims were to establish a comprehensive immunophenotypic spectrum of normal basophils by routinely used markers in the clinical flow cytometry laboratory, to assess the range of immunophenotypic aberrations of basophils in CML, and finally to identify the differential immunophenotype that allows discrimination of basophils from myeloblasts.
MATERIALS AND METHODS
We analyzed the immunophenotype of basophils from 10 peripheral blood specimens from donors without neoplasia, 10 bone marrow samples taken for lymphoma staging (all negative for lymphoma), and 15 CML cases ranging from chronic to blast phases. The diagnosis of CML was made using a combination of morphologic, cytogenetic, and molecular studies. The accelerated and blast phases were defined according to the World Health Organization classification. (12) All samples were evaluated by 4-color staining and acquired on a FACSCalibur flow cytometry instrument with CellQuest Pro software (BD Biosciences, San Jose, Calif). Typically, 50000 total events were acquired to obtain adequate numbers of basophils. Bone marrow and peripheral blood processing and antibody staining were performed as previously described. (16) The procedures followed were in accord with the ethical standards established by The University of Texas M. D. Anderson Cancer Center.
Data analysis was performed using Paint-a-Gate software (BD Biosciences). The basophil population (cluster) was identified by its moderate CD45 expression (dimmer than lymphocytes and brighter than myeloblasts) and low side light scatter. The antigen expression was then assessed on basophils using the above combinations of antibodies, which all included CD45 in each tube. The level/pattern of the antigen expression in control samples was considered as the normal immunophenotype. Percentages of various cell types were determined based on total events. Aberrant basophilic immunophenotypes in CML were defined as at least a half-log shift of the basophil population (decreased or increased antigen expression) compared with basophils in negative control peripheral blood and lymphoma staging bone marrow samples.
Immunophenotype of Basophils in Nonneoplastic Peripheral Blood/Bone Marrow Samples
Immunophenotypic analysis of basophils was performed in peripheral blood from 10 donors without neoplasia and in 10 bone marrow specimens from patients with a history of non-Hodgkin lymphoma. This group included 12 men and 8 women, aged 11 to 71 years (median, 58 years). All patients had no evidence of lymphomatous involvement in the examined samples at the time of the study. The immunophenotype of basophils was consistent and used to define the range of normal basophilic antigen expression. Basophils in all cases were positive for CD9, CD13, CD22 (dimmer than lymphocytes), CD25 (dim), CD33, CD36, CD38 (bright), CD45 (dimmer than lymphocytes and brighter than myeloblasts), and CD123 (bright), and were negative for CD3, CD4, CD19, CD34, CD64, CD117, and HLA-DR. Of note, the apparent expression of CD36 on basophils may well be due to adherent platelets. In a subset of cases, basophils were positive for CD11b (10/20). Characteristic patterns of antigen expression of normal basophils are shown in Figure 1, A through I (from multiple cases). Morphologic examination revealed that the basophils were predominantly mature.
Immunophenotype of Basophils in Peripheral Blood/Bone Marrow Samples of Chronic Myelogenous Leukemia
The CML patients included 9 men and 6 women, aged 19 to 73 years (median, 61 years); 7 patients were in CML CP, 5 in CML-AP, and 3 in CML-BP. Basophils in the peripheral blood (n = 10) or bone marrow (n = 5) samples ranged from 1% to 41% of total analyzed cells (median, 9%). Compared with the control cases, basophils in subsets of CML cases showed increases or decreases in intensity of most antigens tested (detailed in Table 1, with examples of aberrant expression patterns shown in Figure 2, A through L). The most common aberrancies were underexpression of CD38, followed by aberrant expression of CD64 and underexpression of CD123. The patterns of expression of CD11b, CD36, and CD45 were similar to those of the control cases. In all CML cases, basophils demonstrated 1 to 5 immunophenotypic aberrancies with a mean of 2.8 aberrancies per case. There was no significant increase in the number of aberrancies as CML progressed from chronic phase (mean of 2.6 aberrancies per case) to the aggressive stages of CML-AP or CML-BP (both with a mean of 3.0 aberrancies per case).
Expression of CD34 and CD117 on basophilic lineage cells was observed in 1 and 7 cases, respectively, of which 6 cases were either at CML-AP or CML-BP. Expression of these 2 markers was not regarded as immunophenotypic aberrancy in this study since a subset of basophils in these cases exhibited morphologic features of immaturity. Therefore, CD34 and CD117 presumably represented immature cell markers on basophilic precursors/blasts. These cells are generally large in size with round to slightly indented nuclei, finely dispersed chromatin, frequently 1 or more prominent nucleoli, and coarse deep purple granules, often partially overlapping the nuclei (Figure 3). Myeloblasts were concomitantly increased in these cases, ranging from 2% to 62% (median, 28%).
While myeloblasts shared many of the antigens expressed by basophils, they could be distinguished from basophils on the basis of their distinct immunophenotype (Table 2). Myeloblasts frequently expressed CD34, CD117, and HLA-DR; showed dimmer expression (compared with basophils) of CD38, CD45, and CD123; and lacked expression of CD22 (Table 2; Figure 4, A through F). In contrast, basophils usually lacked expression of CD34 and HLA-DR but expressed CD22. Although some of these characteristic differences in antigen expression were lost due to immunophenotypic aberrancy in CML (for instance, HLA-DR was present in abnormal basophils), in our experience the combination of multiple antigen expression patterns permits reliable discrimination of basophils from myeloblasts in any given case. We recommend the following combinations to distinguish basophils from myeloblasts: CD34/CD123/CD45/CD117, CD38/CD22/ CD45/CD33, and HLA-DR/CD123/CD45/CD33 (in the order FITC/PE/PerCP/APC). We found that for some an tigens, in particular CD22, the FITC-conjugated reagent showed suboptimally dim staining. Either CD22-PE or CD22-APC was preferable to CD22-FITC.
[FIGURE 1 OMITTED]
Expression of CD22 on basophils, located in the "blast gate" on CD45 versus side scatter plots, could lead to misinterpretation of basophils as B-lineage lymphoblasts in a patient with suspected CML-BP. Basophils were consistently negative for CD19, permitting distinction from Blymphoblasts.
Our study confirms and expands earlier observations of the IP of basophils in nonneoplastic conditions by multiparameter flow cytometric immunophenotyping. Basophils consistently express CD9, CD13, CD22, CD25 (dim), CD33, CD36, CD38 (bright), CD45 (dimmer than lymphocytes and brighter than myeloblasts), and CD123 (bright); variably express CD11b; and lack expression of CD19, CD34, CD64, CD117, and HLA-DR. The distinct immunophenotype of strong expression of CD38 and CD123 in conjunction with expression of CD22 is characteristic. Multiparameter flow cytometric immunophenotyping thus provides an objective way to evaluate basophil counts and immunophenotypic aberrancies in myeloid neoplasms. Most antigens employed in this study are used routinely in many clinical flow cytometry laboratories. It should be noted that the IP of basophils in chronic myeloproliferative disease-negative bone marrow samples in this study was derived from patients with a history of lymphoma, but with no evidence of lymphomatous involvement at the time of analysis. However, peripheral blood basophils from donors without neoplasia in our study showed a similar phenotype, and our findings are in general agreement with previous studies. (2,4-8)
In addition to expressing myeloid antigens (CD13, CD33, and CD36), basophils express a number of cytokine receptors, including CD25 (interleukin [IL]-2R[alpha])and CD123 (IL-3R[alpha]). Strong expression of CD123 is in keeping with the essential role played by IL-3 and its receptor in the differentiation and proliferation of basophils. (17-20) Regarding basophil differentiation, CD123 is expressed on basophils from the [CD34.sup.+] immature stage to the CD34-mature peripheral stage. (21) Of note, CD117 (c-Kit), a receptor for stem cell factor, is largely absent on mature basophils. This is in contrast to mast cells, which have a high level of expression, reflecting the differential requirement of these growth factors for mast cell and basophil proliferation and differentiation. (8,22)
Interestingly, basophils also express CD22, a well known B-lineage-associated marker. Human basophils react with some but not all monoclonal antibodies raised against B-cell-derived CD22 proteins, as they have been previously shown to be positive with clones Leu-14 and 5.8HK, but not 4KB128 and B3.2,11 We used clone S-HCL-1 in this study and demonstrated staining of both B cells and basophils with this reagent. The difference in anti-CD22 staining pattern with some clones appears to be related to differences in disulfide bond formation and the subsequent 3-dimensional conformation of the protein, such that some of the epitopes exposed on the B-cell surface are not available for binding in basophils. (10) CD22 expression has been conjectured to begin from a quite undifferentiated stage of common lymphoid and myeloid progenitors. (23) It is speculated that CD22 expressed in basophils may regulate the activation signals stimulated by the antigen/IgE complex through Fc[epsilon]R1, somewhat analogous to its regulation of activation signals in B cells stimulated by antigen through the B-cell receptor/CD79 complex. (24)
The expression of CD9 by basophils in all cases is of interest. CD9 is a member of a superfamily of 4 transmembrane domain proteins. (25) This family of proteins, also known as tetraspanins, is known to form complexes with other cell surface molecules and is thought to be involved in a number of cell functions, including regulating cell adhesion. (9,26) This may contribute to basophil emigration to specific extravascular sites, and ultimately their participation in the allergic reaction.
Having characterized the IP of basophils in nonneoplastic specimens, we next evaluated the IP of basophils in CML, as basophils are consistently increased in this entity; indeed, elevation of the basophil count beyond 20% serves as one of the diagnostic criteria for an accelerated phase of CML.12 Little has been previously described about immunophenotypic aberrancies of basophils in CML. We found in all CML cases that basophils possessed 1 to several immunophenotypic aberrancies, with a mean of 2.8 aberrancies per case (Table 1). The most common aberrancy was underexpression of CD38, followed by aberrant expression of CD64, underexpression of CD123, and aberrant expression of HLA-DR. The latter finding was also observed by Kussick and Wood in non-CML chronic myeloproliferative diseases. (5)
[FIGURE 2 OMITTED]
[FIGURE 3 OMITTED]
[FIGURE 4 OMITTED]
Chronic myelogenous leukemia is known to progress from the initial indolent disease to the aggressive stages, CML-AP or CML-BP, in which blasts, most frequently myeloblasts, are consistently increased. Our study demonstrates that differential expression of CD22, CD45, CD34, CD38, and CD123 permits discrimination of basophils from myeloblasts, since basophils characteristically express bright CD45, CD38, and CD123 compared to myeloblasts, are positive for CD22, and largely lack expression of CD34. Basophils share CD22 expression with precursor B-lymphoblasts but are negative for CD19. While our study did not specifically address this issue, we would expect B-lymphoblasts to lack bright expression of CD123.
Interestingly, in a subset of cases where there is a morphologic increase in basophilic precursors, CD117 is variably expressed on basophils (along with dim CD34 expression in a small subset of basophils in 1 case). Expression of CD117 was previously recognized in acute basophilic leukemia27 and a small subset of KU-812 cells, a basophil cell line. (8) This expression might be due to the fact that basophil-committed progenitors express measurable amounts of CD117/c-Kit or perhaps reflect the stem cell origin of the clone (derived from CML cells).
In conclusion, our study characterizes the immunophenotypic profile of basophils by markers routinely used in the clinical flow cytometry laboratory, such as expression of CD22, CD38 (bright), and CD123 (bright). These findings can aid in discriminating basophils/basophilic precursors from myeloblasts and lymphoblasts. We also identify a spectrum of immunophenotypic aberrancy of basophils in CML, which adds to the current knowledge of immunophenotypic aberrations of myeloid lineage cells and may facilitate the diagnosis of chronic myeloproliferative diseases.
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Xiaohong Han, MD; Jeffrey L. Jorgensen, MD, PhD; Archana Brahmandam, MS; Ellen Schlette, MD; Yang O. Huh, MD; Yuankai Shi, MD, PhD; Sylvester Awagu, DDS; Weina Chen, MD, PhD
Accepted for publication October 29, 2007.
From the Department of Hematopathology, The University of Texas M. D. Anderson Cancer Center, Houston (Drs Han, Jorgensen, Schlette, Huh, and Awagu and Ms Brahmandam); Medical Oncology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China (Dr Shi); and Department of Pathology, The University of Texas Southwestern Medical Center at Dallas (Dr Chen).
The authors have no relevant financial interest in the products or companies described in this article.
Part of this study was published as an abstract (number 1064) at the 95th Annual Meeting of United States and Canadian Academy of Pathology, Atlanta, Ga, 2006.
Reprints: Weina Chen, MD, PhD, UT Southwestern Medical Center, Department of Pathology, 5323 Harry Hines Blvd, Dallas, TX 753909072 (e-mail: firstname.lastname@example.org).
Table 1. Immunophenotypic Aberrancies of Basophils in Chronic Myelogenous Leukemia (CML) * Age, y/Sex CD9 CD13 CD22 CD25 CD33 Normal basophils + + + + + CML-CPt 72/M 65/M 41/M 46/M 36/M - 71/M br+ 73/F - CML-APt 69/F 64/M 45/M pt+ 28/M br+ - 61/F Dim+ - CML-BPt 19/F - 28/F pt+ - 62/F pt+ ND Overall aberrancies 3/15 2/15 3/15 3/14 1/15 Age, y/Sex CD38 CD64 CD123 HLA-DR Normal basophils br+ - br+ - CML-CPt 72/M Dim+ pt+ 65/M Dim+ pt+ 41/M Dim+ pt+ 46/M Dim+ pt+ 36/M Dim+ Dim+ 71/M pt+ pt+ 73/F Dim+ + Dim+ CML-APt 69/F Dim+ 64/M Dim+ 45/M Dim+ Dim+ 28/M Dim+ pt+ pt+ 61/F Dim+ Dim+ + CML-BPt 19/F Dim+ 28/F Dim+ 62/F Dim+ Dim+ + Overall aberrancies 13/15 8/15 5/15 4/15 Aberrancies/ Age, y/Sex Case Normal basophils CML-CPt 72/M 2 65/M 2 41/M 2 46/M 2 36/M 3 71/M 3 73/F 4 CML-APt 69/F 1 64/M 1 45/M 3 28/M 5 61/F 5 CML-BPt 19/F 2 28/F 3 62/F 4 Overall aberrancies Mean, 2.8 * + indicates positive; br, bright;--, negative; CP, chronic phase; pt, partial; AP, accelerated phase; BP, blast phase; and ND, not done. ([dagger]) Only aberrancies in antigen expression are listed. Table 2. Differential Antigen Expression Among Normal Basophils, Basophils/Basophilic Precursors, and Myeloblasts in Chronic Myelogenous Leukemia (CML) * Antigen Normal Basophils/Basophilic Myeloblasts Expression Basophils Precursors in CML in CML CD22 + +/- - CD34 - -/+ +/- CD38 Bright+ Dim + Dim + CD45 Moderate + Moderate+ Dim + CD64 - +/- - CD117 - -/+ CD123 Bright+ Dim to strong+ Dim + HLA-DR - -/+ + * + indicates antigen consistently expressed; +/-, antigen expressed in most cases; -, lack of expression or antigen consistently negative; and -/+, antigen frequently lost.
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