<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Iranian Biomedical Journal</title>
<title_fa>مجله بیومدیکال ایران</title_fa>
<short_title>IBJ</short_title>
<subject>Basic Sciences</subject>
<web_url>http://ibj.pasteur.ac.ir</web_url>
<journal_hbi_system_id>1</journal_hbi_system_id>
<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>1028-852X</journal_id_issn>
<journal_id_issn_online>2008-823X</journal_id_issn_online>
<journal_id_pii>-</journal_id_pii>
<journal_id_doi>10.61882/ibj</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid>-</journal_id_sid>
<journal_id_nlai>8888</journal_id_nlai>
<journal_id_science>-</journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1376</year>
	<month>7</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>1997</year>
	<month>10</month>
	<day>1</day>
</pubdate>
<volume>1</volume>
<number>4</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa>Detection of Pre-Malifnant B-1 Cells in NZB Mice with a Re-stricted CDR3/DFL16 Region</title_fa>
	<title>Detection of Pre-Malifnant B-1 Cells in NZB Mice with a Re-stricted CDR3/DFL16 Region</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa>مقاله کامل</content_type_fa>
	<content_type>Full Length/Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>The relationship between the immunoglobulin (Ig) nucleotide sequence and the ability of a B cell to develop into a malignant cell was studied in a subset of B cells, B-1 cells. B-1 cells become malignant in chronic lymphocytic leukemia (CLL) and are responsible for the production of &amp;quot;natural autoanti&#8204;bodies&amp;quot;. The autoimmune NZB mouse has been known as a human malignancy and CLL model, be&#8204;cause of the age-dependent onset of clonally expanded hyperdiploid B-1 cells in these mice. The Ig heavy chain variable region in hyperdiploid B-1 clones from several NZB mice showed common char&#8204;acteristics in the CDR3 shared with fetal B cells: lack of N base insertions and presence of homology sequences at the VH-D-JH junctions that can be encoded by either of the two joined gene segments. Using a degenerative oligoprimer was shown no significant differences in expression of the restricted CDR3/DFL16 region in newborns or in the liver of either strain of mice as young adults. However, the expression of the restricted CDR3/DFL16 in the spleens of young adult NZB was remarkably ele&#8204;vated and showed significant differences from the expression in newborn NZB as well as from young adult and newborn BALB/c mice. It appears that malignant hyperdiploid B-1 cells are derived from fetal B cells. This technique can be used as a molecular marker to demonstrate a relative increase in the expression of this CDR3 in animals pre-destined to develop B-malignancies.</abstract>
	<keyword_fa></keyword_fa>
	<keyword>pre-malignant B-1 cells, CDR3, junctional homology, quantitative PCR</keyword>
	<start_page>27</start_page>
	<end_page>34</end_page>
	<web_url>http://ibj.pasteur.ac.ir/browse.php?a_code=A-10-1-444&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Fereidoun</first_name>
	<middle_name></middle_name>
	<last_name>Mahboudi</last_name>
	<suffix></suffix>
	<first_name_fa>فریدون</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>مهبودی</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code></code>
	<orcid></orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation></affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Ann. J,</first_name>
	<middle_name></middle_name>
	<last_name>Feeney</last_name>
	<suffix></suffix>
	<first_name_fa>Elizabeth</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>Ravech</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code></code>
	<orcid></orcid>
	<coreauthor>No</coreauthor>
	<affiliation></affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Larry </first_name>
	<middle_name></middle_name>
	<last_name>Arnold</last_name>
	<suffix></suffix>
	<first_name_fa>Geoffrey</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>Haughton</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code></code>
	<orcid></orcid>
	<coreauthor>No</coreauthor>
	<affiliation></affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Geoffrey</first_name>
	<middle_name></middle_name>
	<last_name>Haughton</last_name>
	<suffix></suffix>
	<first_name_fa>Larry</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>Arnold</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code></code>
	<orcid></orcid>
	<coreauthor>No</coreauthor>
	<affiliation></affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Elizabeth</first_name>
	<middle_name></middle_name>
	<last_name>Ravech</last_name>
	<suffix></suffix>
	<first_name_fa>Ann. J,</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>Feeney</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code></code>
	<orcid></orcid>
	<coreauthor>No</coreauthor>
	<affiliation></affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
