Dear Juan,
Neutrophils express CD64, the high affinity receptor for IgG upon G-CSF
treatment, resulting in high background and unspecific staining (hard to get
rid off by blocking steps). The other population you described are normal B
cell precursors in the bone marrow.
Regards
Thomas Nebe
Dr.med. C. Thomas Nebe
Universitaetsklinikum Mannheim
Zentrallabor
Theodor-Kutzer-Ufer 1-3
D-68167 Mannheim
Tel. +49 621 383-3485
FAX +49 621 383-73 3485
+49 621 383-3819
e-mail: thomas.nebe@ikc.ma.uni-heidelberg.de
Bitte besuchen Sie unsere sehr informativen Webseiten unter
http://www.ma.uni-heidelberg.de/inst/ikc/
> -----Ursprüngliche Nachricht-----
> Von: Gerhard Nebe-von-Caron [SMTP:Gerhard.Nebe-von-Caron@unilever.com]
> Gesendet am: Mittwoch, 20. Oktober 1999 17:07
> An: Nebe, Thomas C.
> Betreff: FW: KOSTMANN`S NEUTROPENIA
>
>
>
> -----Original Message-----
> From: JUAN LUIS CASTILLO NAVARRETE [SMTP:axelyoyi@entelchile.net]
> Sent: Tuesday, October 19, 1999 5:12 AM
> To: Cytometry Mailing List
> Subject: KOSTMANN`S NEUTROPENIA
>
>
> HI FLOWERS:
>
> Today I have a immunphenotyping of a patient,a male,4 years, the sample
> was bone marrow (als periphereal blood), and the diagnosis was
> Kostmann`s neutropenia. Also the patient is under treatment with G-CSF.
> In the immunophenotyping I found a few things that not are clear for me:
> the netrophil population have a normal FSC but have a low SSC, and also
> have normal markers for myeloid (CD33, CD13, MPO, TDT), but also have a
> expression of CD61 (M7?). Also I found a little population of cells with
> low SSC and Low expression of CD45 (the classical region of blast). This
> cells was CD19, CD20, HLA-DR, CD10(CALLA), MPO dim, TDT(-), CD61(-),
> CD34 (-), CD33 (-), CD13 (-), CD14(-).
> I search information about Kostmann`s syndrome, and the next is the
> principal:
>
> Severe congenital neutropenia (SCN) or Kostmann's syndrome is
> characterized by a stop in differentiation of myeloid progenitor cells
> at the myelocytic or promyelocytic stage. with absence of neutrophils in
> bone marrow (BM) and blood. The pathophysiology of SCN is still
> unclear. (Exp Hematol 1999 Jun; 27(6):1038-45.
> Hypotheses of the pathophysiology of SCN include (1) defective
> production of granulocyte colony-stimulating factor (G-CSF), and/or (2)
> defective response to G-CSF. (Blood 1991 May; 77(9):1919-22).
> The administration of granulocyte- colony-stimulating factor was shown
> to be safe and effective also in reducing infectious episodes in these
> patients. (Acta Paediatr 1992 Feb; 81(2):133-6).
> Thus, it is hypothesized that the underlying defect responsible for
> SCN is based on an abnormal G-CSF-induced signal transduction pathway
> .eutrophils from SCN patients show an increased autophosphorylation of
> JAK2 (a nonreceptor tyrosine kinase involved in the signaling pathway of
> G-CSF )in comparison with that of neutrophils from healthy volunteers.
> (Blood 1995 Dec; 86(12):4500-5).
>
>
> So, the patient : May be a leukemia ? , M7 ? , lymphoid ? or Does the
> normal production of bone marrow upon treatment of G-CSF ?
>
> Any idea will helpme
>
> Thanks
>
>
> JUAN LUIS CASTILLO N.
> CITOMETRIA DE FLUJO
> HOSPITAL DEL TRABAJADOR
> CONCEPCION
> CHILE
> PHONE: 56-41-201722
> FAX: 56-41-311008
> EMAIL: axelyoyi@entelchile.net
>
> << Datei: ATT01413.ATT >>
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