Inefficient processing of mRNA for the membraneform of IgE is a genetic mechanism to limit recruitment of IgE‐secreting cells
Immunoglobulin E (IgE) is the key effector element in allergic diseases ranging from innocuous hay fever to life‐threatening anaphylactic shock. Compared to other Ig classes, IgE serum levels are very low. In its membrane‐bound form (mIgE), IgE behaves as a classical antigen receptor on B lymphocyte...
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Published in | European Journal of Immunology Vol. 36; no. 7; pp. 1917 - 1925 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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WILEY‐VCH Verlag
01.07.2006
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Abstract | Immunoglobulin E (IgE) is the key effector element in allergic diseases ranging from innocuous hay fever to life‐threatening anaphylactic shock. Compared to other Ig classes, IgE serum levels are very low. In its membrane‐bound form (mIgE), IgE behaves as a classical antigen receptor on B lymphocytes. Expression of mIgE is essential for subsequent recruitment of IgE‐secreting cells. We show that in activated, mIgE‐bearing B cells, mRNA for the membrane forms of both murine and human epsilon (ϵ) heavy chains (HC) are poorly expressed compared to mRNA for the secreted forms. In contrast, in mIgG‐bearing B cells, mRNA for the membrane forms of murine gamma‐1 (γ1) and the corresponding human γ4 HC are expressed at a much higher level than mRNA for the respective secreted forms. We show that these findings correlate with the presence of deviant polyadenylation signal hexamers in the 3′ untranslated region (UTR) of both murine and human ϵ genes, causing inefficient processing of primary transcripts and thus poor expression of the proteins and poor recruitment of IgE‐producing cells in the immune response. Thus, we have identified a genetic steering mechanism in the regulation of IgE synthesis that represents a further means to restrain potentially dangerous, high serum IgE levels. |
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AbstractList | Immunoglobulin E (IgE) is the key effector element in allergic diseases ranging from innocuous hay fever to life‐threatening anaphylactic shock. Compared to other Ig classes, IgE serum levels are very low. In its membrane‐bound form (mIgE), IgE behaves as a classical antigen receptor on B lymphocytes. Expression of mIgE is essential for subsequent recruitment of IgE‐secreting cells. We show that in activated, mIgE‐bearing B cells, mRNA for the membrane forms of both murine and human epsilon (ϵ) heavy chains (HC) are poorly expressed compared to mRNA for the secreted forms. In contrast, in mIgG‐bearing B cells, mRNA for the membrane forms of murine gamma‐1 (γ1) and the corresponding human γ4 HC are expressed at a much higher level than mRNA for the respective secreted forms. We show that these findings correlate with the presence of deviant polyadenylation signal hexamers in the 3′ untranslated region (UTR) of both murine and human ϵ genes, causing inefficient processing of primary transcripts and thus poor expression of the proteins and poor recruitment of IgE‐producing cells in the immune response. Thus, we have identified a genetic steering mechanism in the regulation of IgE synthesis that represents a further means to restrain potentially dangerous, high serum IgE levels. ImmunoglobulinE (IgE) is the key effector element in allergic diseases ranging from innocuous hay fever to life-threatening anaphylactic shock. Compared to other Ig classes, IgE serum levels are very low. In its membrane-bound form (mIgE), IgE behaves as a classical antigen receptor on Blymphocytes. Expression of mIgE is essential for subsequent recruitment of IgE-secreting cells. We show that in activated, mIgE-bearing Bcells, mRNA for the membrane forms of both murine and human epsilon () heavy chains (HC) are poorly expressed compared to mRNA for the secreted forms. In contrast, in mIgG-bearing Bcells, mRNA for the membrane forms of murine gamma-1 (1) and the corresponding human 4 HC are expressed at a much higher level than mRNA for the respective secreted forms. We show that these findings correlate with the presence of deviant polyadenylation signal hexamers in the 3untranslated region (UTR) of both murine and human genes, causing inefficient processing of primary transcripts and thus poor expression of the proteins and poor recruitment of IgE-producing cells in the immune response. Thus, we have identified a genetic steering mechanism in the regulation of IgE synthesis that represents a further means to restrain potentially dangerous, high serum IgE levels. |
Author | Lamers, Marinus C. Karnowski, Alexander Achatz‐Straussberger, Gertrude Klockenbusch, Cordula Achatz, Gernot |
Author_xml | – sequence: 1 givenname: Alexander surname: Karnowski fullname: Karnowski, Alexander – sequence: 2 givenname: Gertrude surname: Achatz‐Straussberger fullname: Achatz‐Straussberger, Gertrude – sequence: 3 givenname: Cordula surname: Klockenbusch fullname: Klockenbusch, Cordula – sequence: 4 givenname: Gernot surname: Achatz fullname: Achatz, Gernot – sequence: 5 givenname: Marinus C. surname: Lamers fullname: Lamers, Marinus C. email: lamers@immunbio.mpg.de |
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Snippet | Immunoglobulin E (IgE) is the key effector element in allergic diseases ranging from innocuous hay fever to life‐threatening anaphylactic shock. Compared to... ImmunoglobulinE (IgE) is the key effector element in allergic diseases ranging from innocuous hay fever to life-threatening anaphylactic shock. Compared to... |
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SubjectTerms | Allergy B cell Class switch Immune response Polyadenylation |
Title | Inefficient processing of mRNA for the membraneform of IgE is a genetic mechanism to limit recruitment of IgE‐secreting cells |
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