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Monocyte
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===Monocytosis=== [[Monocytosis]] is the state of excess monocytes in the peripheral blood. It may be indicative of various disease states. Examples of processes that can increase a monocyte count include: * [[chronic inflammation]] * [[diabetes]]<ref>{{cite journal |last1=Hoyer |first1=FF |last2=Zhang |first2=X |last3=Coppin |first3=E |last4=Vasamsetti |first4=SB |last5=Modugu |first5=G |last6=Schloss |first6=MJ |last7=Rohde |first7=D |last8=McAlpine |first8=CS |last9=Iwamoto |first9=Y |last10=Libby |first10=P |last11=Naxerova |first11=K |last12=Swirski |first12=F |last13=Dutta |first13=P |last14=Nahrendorf |first14=P |title=Bone Marrow Endothelial Cells Regulate Myelopoiesis in Diabetes |journal=Circulation |date=April 2020 |volume=142 |issue=3 |pages=244–258 |doi=10.1161/CIRCULATIONAHA.120.046038 |pmid=32316750|pmc=7375017 }}</ref> * [[Stress (medicine)|stress]] response<ref>{{cite journal |last1=Heidt |first1=Timo |last2=Sager |first2=Hendrik B |last3=Courties |first3=Gabriel |last4=Dutta |first4=Partha |last5=Iwamoto |first5=Yoshiko |last6=Zaltsman |first6=Alex |last7=von zur Muhlen |first7=Constantin |last8=Bode |first8=Christoph |last9=Fricchione |first9=Gregory L |last10=Denninger |first10=John |last11=Lin |first11=Charles P |last12=Vinegoni |first12=Claudio |last13=Libby |first13=Peter |last14=Swirski |first14=Filip K |last15=Weissleder |first15=Ralph |last16=Nahrendorf |first16=Matthias |title=Chronic variable stress activates hematopoietic stem cells |journal=Nature Medicine |date=July 2014 |volume=20 |issue=7 |pages=754–758 |doi=10.1038/nm.3589 |pmid=24952646 |pmc=4087061 }}</ref> * [[Cushing's syndrome]] (hyperadrenocorticism) * [[immune-mediated disease]] * [[granuloma]]tous disease * [[atherosclerosis]]<ref>{{cite journal |last1=Swirski |first1=Filip K. |last2=Libby |first2=Peter |last3=Aikawa |first3=Elena |last4=Alcaide |first4=Pilar |last5=Luscinskas |first5=F. William |last6=Weissleder |first6=Ralph |last7=Pittet |first7=Mikael J. |date=2 January 2007 |title=Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata |journal=[[Journal of Clinical Investigation]] |volume=117 |issue=1 |pages=195–205 |doi=10.1172/JCI29950 |pmc=1716211 |pmid=17200719}}</ref> * [[necrosis]] * [[red blood cell]] regeneration * [[viral fever]] * [[sarcoidosis]] * [[chronic myelomonocytic leukemia]] (CMML) * Resolution of [[fasting]]<ref name="i205">{{cite journal | last1=O’Brien | first1=Conan J.O. | last2=Domingos | first2=Ana I. | title=Old and "hangry" monocytes turn from friend to foe under assault | journal=Immunity | volume=56 | issue=4 | date=2023 | doi=10.1016/j.immuni.2023.03.013 | pages=747–749| pmid=37044065 }}</ref> A high count of CD14<sup>+</sup>CD16<sup>++</sup> monocytes is found in severe infection ([[sepsis]]).<ref>{{cite journal |last1=Fingerle |first1=G |last2=Pforte |first2=A |last3=Passlick |first3=B |last4=Blumenstein |first4=M |last5=Strobel |first5=M |last6=Ziegler- Heitbrock |first6=Hw |title=The novel subset of CD14+/CD16+ blood monocytes is expanded in sepsis patients |journal=Blood |date=15 November 1993 |volume=82 |issue=10 |pages=3170–3176 |doi=10.1182/blood.v82.10.3170.3170 |pmid=7693040 |doi-access=free }}</ref> In the field of atherosclerosis, high numbers of the CD14<sup>++</sup>CD16<sup>+</sup> intermediate monocytes were shown to be predictive of cardiovascular events in populations at risk.<ref>{{cite journal |last1=Heine |first1=G.H. |last2=Ulrich |first2=C. |last3=Seibert |first3=E. |last4=Seiler |first4=S. |last5=Marell |first5=J. |last6=Reichart |first6=B. |last7=Krause |first7=M. |last8=Schlitt |first8=A. |last9=Köhler |first9=H. |last10=Girndt |first10=M. |date=March 2008 |title=CD14++CD16+ monocytes but not total monocyte numbers predict cardiovascular events in dialysis patients |journal=[[Kidney International]] |volume=73 |issue=5 |pages=622–629 |doi=10.1038/sj.ki.5002744 |pmid=18160960 |doi-access=free}}</ref><ref>{{cite journal |last1=Rogacev |first1=Kyrill S. |last2=Cremers |first2=Bodo |last3=Zawada |first3=Adam M. |last4=Seiler |first4=Sarah |last5=Binder |first5=Nadine |last6=Ege |first6=Philipp |last7=Große-Dunker |first7=Gunnar |last8=Heisel |first8=Isabel |last9=Hornof |first9=Florian |last10=Jeken |first10=Jana |last11=Rebling |first11=Niko M. |date=October 2012 |title=CD14++CD16+ Monocytes Independently Predict Cardiovascular Events |journal=[[Journal of the American College of Cardiology]] |volume=60 |issue=16 |pages=1512–1520 |doi=10.1016/j.jacc.2012.07.019 |pmid=22999728 |doi-access=free |last12=Ulrich |first12=Christof |last13=Scheller |first13=Bruno |last14=Böhm |first14=Michael |last15=Fliser |first15=Danilo |last16=Heine |first16=Gunnar H.}}</ref> CMML is characterized by a persistent monocyte count of > 1000/microL of blood. Analysis of monocyte subsets has demonstrated predominance of classical monocytes and absence of CD14lowCD16+ monocytes.<ref>{{cite journal |last1=Vuckovic |first1=S. |last2=Fearnley |first2=D. B. |last3=Gunningham |first3=S. |last4=Spearing |first4=R. L. |last5=Patton |first5=W. N. |last6=Hart |first6=D. N. J. |date=June 1999 |title=Dendritic cells in chronic myelomonocytic leukaemia: Dendritic Cells in CMML |journal=[[British Journal of Haematology]] |volume=105 |issue=4 |pages=974–985 |doi=10.1046/j.1365-2141.1999.01431.x |pmid=10554809 |doi-access=free |s2cid=22571555}}</ref><ref>{{cite journal |last1=Selimoglu-Buet |first1=Dorothée |last2=Wagner-Ballon |first2=Orianne |last3=Saada |first3=Véronique |last4=Bardet |first4=Valérie |last5=Itzykson |first5=Raphaël |last6=Bencheikh |first6=Laura |last7=Morabito |first7=Margot |last8=Met |first8=Elisabeth |last9=Debord |first9=Camille |last10=Benayoun |first10=Emmanuel |last11=Nloga |first11=Anne-Marie |last12=Fenaux |first12=Pierre |last13=Braun |first13=Thorsten |last14=Willekens |first14=Christophe |last15=Quesnel |first15=Bruno |last16=Adès |first16=Lionel |last17=Fontenay |first17=Michaela |last18=Rameau |first18=Philippe |last19=Droin |first19=Nathalie |last20=Koscielny |first20=Serge |last21=Solary |first21=Eric |title=Characteristic repartition of monocyte subsets as a diagnostic signature of chronic myelomonocytic leukemia |journal=Blood |date=4 June 2015 |volume=125 |issue=23 |pages=3618–3626 |doi=10.1182/blood-2015-01-620781 |pmid=25852055 |pmc=4497970 }}</ref> The absence of non-classical monocytes can assist in diagnosis of the disease and the use of slan as a marker can improve specificity.<ref>{{cite journal |last1=Tarfi |first1=Sihem |last2=Badaoui |first2=Bouchra |last3=Freynet |first3=Nicolas |last4=Morabito |first4=Margot |last5=Lafosse |first5=Jeffie |last6=Toma |first6=Andréa |last7=Etienne |first7=Gabriel |last8=Micol |first8=Jean-Baptiste |last9=Sloma |first9=Ivan |last10=Fenaux |first10=Pierre |last11=Solary |first11=Eric |date=April 2020 |title=Disappearance of slan-positive non-classical monocytes for diagnosis of chronic myelomonocytic leukemia with an associated inflammatory state |journal=[[Haematologica]] |volume=105 |issue=4 |pages=e147–e152 |doi=10.3324/haematol.2019.219782 |pmid=31413091 |doi-access=free |last12=Selimoglu-Buet |first12=Dorothée |last13=Wagner-Ballon |first13=Orianne |s2cid=199663779}}</ref>
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